sample case study pregnancy induced hypertension

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• v.6(2); 2009 Feb

A 21-Year-Old Pregnant Woman with Hypertension and Proteinuria

Ronald Ma and colleagues describe the differential diagnosis, investigation, and management of a 21-year-old pregnant woman presenting with hypertension and proteinuria at 20 weeks of gestation.

DESCRIPTION of CASE

A 21-year-old pregnant woman, gravida 2 para 1, presented with hypertension and proteinuria at 20 weeks of gestation. She had a history of pre-eclampsia in her first pregnancy one year ago. During that pregnancy, at 39 weeks of gestation, she developed high blood pressure, proteinuria, and deranged liver function. She eventually delivered by emergency caesarean section following failed induction of labour. Blood pressure returned to normal post-partum and she received no further medical follow-up. Family history was remarkable for her mother's diagnosis of hypertension in her fourth decade. Her father and five siblings, including a twin sister, were healthy. She did not smoke nor drink any alcohol. She was not taking any regular medications, health products, or herbs.

At 20 weeks of gestation, blood pressure was found to be elevated at 145/100 mmHg during a routine antenatal clinic visit. Aside from a mild headache, she reported no other symptoms. On physical examination, she was tachycardic with heart rate 100 beats per minute. Body mass index was 16.9 kg/m 2 and she had no cushingoid features. Heart sounds were normal, and there were no signs suggestive of congestive heart failure. Radial-femoral pulses were congruent, and there were no audible renal bruits.

Baseline laboratory investigations showed normal renal and liver function with normal serum urate concentration. Random glucose was 3.8 mmol/l. Complete blood count revealed microcytic anaemia with haemoglobin level 8.3 g/dl (normal range 11.5–14.3 g/dl) and a slightly raised platelet count of 446 × 10 9 /l (normal range 140–380 × 10 9 /l). Iron-deficient state was subsequently confirmed. Quantitation of urine protein indicated mild proteinuria with protein:creatinine ratio of 40.6 mg/mmol (normal range <30 mg/mmol in pregnancy).

What Were Our Differential Diagnoses?

An important cause of hypertension that occurs during pregnancy is pre-eclampsia. It is a condition unique to the gravid state and is characterised by the onset of raised blood pressure and proteinuria in late pregnancy, at or after 20 weeks of gestation [ 1 ]. Pre-eclampsia may be associated with hyperuricaemia, deranged liver function, and signs of neurologic irritability such as headaches, hyper-reflexia, and seizures. In our patient, hypertension developed at a relatively early stage of pregnancy than is customarily observed in pre-eclampsia. Although she had proteinuria, it should be remembered that this could also reflect underlying renal damage due to chronic untreated hypertension. Additionally, her electrocardiogram showed left ventricular hypertrophy, which was another indicator of chronicity.

While pre-eclampsia might still be a potential cause of hypertension in our case, the possibility of pre-existing hypertension needed to be considered. Box 1 shows the differential diagnoses of chronic hypertension, including essential hypertension, primary hyperaldosteronism related to Conn's adenoma or bilateral adrenal hyperplasia, Cushing's syndrome, phaeochromocytoma, renal artery stenosis, glomerulopathy, and coarctation of the aorta.

Box 1: Causes of Hypertension in Pregnancy

• Pre-eclampsia
• Essential hypertension
• Renal artery stenosis
• Glomerulopathy
• Renal parenchyma disease
• Primary hyperaldosteronism (Conn's adenoma or bilateral adrenal hyperplasia)
• Cushing's syndrome
• Phaeochromocytoma
• Coarctation of aorta
• Obstructive sleep apnoea

Renal causes of hypertension were excluded based on normal serum creatinine and a bland urinalysis. Serology for anti-nuclear antibodies was negative. Doppler ultrasonography of renal arteries showed normal flow and no evidence of stenosis. Cushing's syndrome was unlikely as she had no clinical features indicative of hypercortisolism, such as moon face, buffalo hump, violaceous striae, thin skin, proximal muscle weakness, or hyperglycaemia. Plasma potassium concentration was normal, although normokalaemia does not rule out primary hyperaldosteronism. Progesterone has anti-mineralocorticoid effects, and increased placental production of progesterone may mask hypokalaemia. Besides, measurements of renin activity and aldosterone concentration are difficult to interpret as the renin-angiotensin-aldosterone axis is typically stimulated in pregnancy. Phaeochromocytoma is a rare cause of hypertension in pregnancy that, if unrecognised, is associated with significant maternal and foetal morbidity and mortality. The diagnosis can be established by measuring levels of catecholamines (noradrenaline and adrenaline) and/or their metabolites (normetanephrine and metanephrine) in plasma or urine.

What Was the Diagnosis?

Catecholamine levels in 24-hour urine collections were found to be markedly raised. Urinary noradrenaline excretion was markedly elevated at 5,659 nmol, 8,225 nmol, and 9,601 nmol/day in repeated collections at 21 weeks of gestation (normal range 63–416 nmol/day). Urinary adrenaline excretion was normal. Pregnancy may induce mild elevation of catecholamine levels, but the marked elevation of urinary catecholamine observed was diagnostic of phaeochromocytoma. Conditions that are associated with false positive results, such as acute myocardial infarction, congestive heart failure, acute cerebrovascular event, withdrawal from alcohol, withdrawal from clonidine, and cocaine abuse, were not present in our patient.

The working diagnosis was therefore phaeochromocytoma complicating pregnancy. Magnetic resonance imaging (MRI) of neck to pelvis, without gadolinium enhancement, was performed at 24 weeks of gestation. It showed a 4.2 cm solid lesion in the mid-abdominal aorto-caval region, while both adrenals were unremarkable. There were no ectopic lesions seen in the rest of the examined areas. Based on existing investigation findings, it was concluded that she had extra-adrenal paraganglioma resulting in hypertension.

What Was the Next Step in Management?

At 22 weeks of gestation, the patient was started on phenoxybenzamine titrated to a dose of 30 mg in the morning and 10 mg in the evening. Propranolol was added several days after the commencement of phenoxybenzamine. Apart from mild postural dizziness, the medical therapy was well tolerated during the remainder of the pregnancy. In the third trimester, systolic and diastolic blood pressures were maintained to below 90 mmHg and 60 mmHg, respectively. During this period, she developed mild elevation of alkaline phosphatase ranging from 91 to 188 IU/l (reference 35–85 IU/l). However, liver transaminases were normal and the patient had no seizures. Repeated urinalysis showed resolution of proteinuria. At 38 weeks of gestation, the patient proceeded to elective caesarean section because of previous caesarean section, and a live female baby weighing 3.14 kg was delivered. The delivery was uncomplicated and blood pressure remained stable.

Following the delivery, computer tomography (CT) scan of neck, abdomen, and pelvis was performed as part of pre-operative planning to better delineate the relationship of the tumour to neighbouring structures. In addition to the previously identified extra-adrenal paraganglioma in the abdomen ( Figure 1 ), the CT revealed a 9 mm hypervascular nodule at the left carotid bifurcation, suggestive of a carotid body tumour ( Figure 2 ). The patient subsequently underwent an iodine (I) 131 metaiodobenzylguanidine (MIBG) scan, which demonstrated marked MIBG-avidity of the paraganglioma in the mid-abdomen. The reported left carotid body tumour, however, did not demonstrate any significant uptake. This could indicate either that the MIBG scan had poor sensitivity in detecting a small tumour, or that the carotid body tumour was not functional.

In June 2008, four months after the delivery, the patient had a laparotomy with removal of the abdominal paraganglioma. The operation was uncomplicated. There was no wide fluctuation of blood pressures intra- and postoperatively. Phenoxybenzamine and propranolol were stopped after the operation. Histology of the excised tumour was consistent with paraganglioma with cells staining positive for chromogranin ( Figures 3 and ​ and4) 4 ) and synaptophysin. Adrenal tissues were notably absent.

The tumour is a well-circumscribed fleshy yellowish mass with maximal dimension of 5.5 cm.

The tumour cells are polygonal with bland nuclei. The cells are arranged in nests and are immunoreactive to chromogranin (shown here) and synaptophysin.

The patient was counselled for genetic testing for hereditary phaeochromocytoma/paraganglioma. She was found to be heterozygous for c.449_453dup mutation of the succinate dehydrogenase subunit D (SDHD) gene ( Figure 5 ). This mutation is a novel frameshift mutation, and leads to SDHD deficiency (GenBank accession number: 1162563). At the latest clinic visit in August 2008, she was asymptomatic and normotensive. Measurements of catecholamine in 24-hour urine collections had normalised. Resection of the left carotid body tumour was planned for a later date. She was to be followed up indefinitely to monitor for recurrences. She was also advised to contact family members for genetic testing. Our patient gave written consent for this case to be published.

Phaeochromocytoma in Pregnancy

Hypertension during pregnancy is a frequently encountered obstetric complication that occurs in 6%–8% of pregnancies [ 2 ]. Phaeochromocytoma presenting for the first time in pregnancy is rare, and only several hundred cases have been reported in the English literature. In a recent review of 41 cases that presented during 1988 to 1997, maternal mortality was 4% while the rate of foetal loss was 11% [ 3 ]. Antenatal diagnosis was associated with substantial reduction in maternal mortality but had little impact on foetal mortality. Further, chronic hypertension, regardless of aetiology, increases the risk of pre-eclampsia by 10-fold [ 1 ].

Classically, patients with phaeochromocytoma present with spells of palpitation, headaches, and diaphoresis [ 4 ]. Hypertension may be sustained or sporadic, and is associated with orthostatic blood pressure drop because of hypovolaemia and impaired vasoconstricting response to posture change. During pregnancy, catecholamine surge may be triggered by pressure from the enlarging uterus and foetal movements. In the majority of cases, catecholamine-secreting tumours develop in the adrenal medulla and are termed phaeochromocytoma. Ten percent of tumours arise from extra-adrenal chromaffin tissues located in the abdomen, pelvis, or thorax to form paraganglioma that may or may not be biochemically active. The malignant potential of phaeochromocytoma or paraganglioma cannot be determined from histology and is inferred by finding tumours in areas of the body not known to contain chromaffin tissues. The risk of malignancy is higher in extra-adrenal tumours and in tumours that secrete dopamine.

Making the Correct Diagnosis

The diagnosis of phaeochromocytoma requires a combination of biochemical and anatomical confirmation. Catecholamines and their metabolites, metanephrines, can be easily measured in urine or plasma samples. Day collection of urinary fractionated metanephrine is considered the most sensitive in detecting phaeochromocytoma [ 5 ]. In contrast to sporadic release of catecholamine, secretion of metanephrine is continuous and is less subjective to momentary stress. Localisation of tumour can be accomplished by either CT or MRI of the abdomen [ 6 ]. Sensitivities are comparable, although MRI is preferable in pregnancy because of minimal radiation exposure. Once a tumour is identified, nuclear medicine imaging should be performed to determine its activity, as well as to search for extra-adrenal diseases. I 131 or I 123 MIBG scan is the imaging modality of choice. Metaiodobenzylguanidine structurally resembles noradrenaline and is concentrated in chromaffin cells of phaeochromocytoma or paraganglioma that express noradrenaline transporters. Radionucleotide imaging is contraindicated in pregnancy and should be deferred until after the delivery.

Treatment Approach

Upon confirming the diagnosis, medical therapy should be initiated promptly to block the cardiovascular effects of catecholamine release. Phenoxybenzamine is a long-acting non-selective alpha-blocker commonly used in phaeochromocytoma to control blood pressure and prevent cardiovascular complications [ 7 ]. The main side-effects of phenoxybenzamine are postural hypotension and reflex tachycardia. The latter can be circumvented by the addition of a beta-blocker. It is important to note that beta-blockers should not be used in isolation, since blockade of ß2-adrenoceptors, which have a vasodilatory effect, can cause unopposed vasoconstriction by a1-adrenoceptor stimulation and precipitate severe hypertension. There is little data on the safety of use of phenoxybenzamine in pregnancy, although its use is deemed necessary and probably life-saving in this precarious situation.

The definitive treatment of phaeochromocytoma or paraganglioma is surgical excision. The timing of surgery is critical, and the decision must take into consideration risks to the foetus, technical difficulty regarding access to the tumour in the presence of a gravid uterus, and whether the patient's symptoms can be satisfactorily controlled with medical therapy [ 8 , 9 ]. It has been suggested that surgical resection is reasonable if the diagnosis is confirmed and the tumour identified before 24 weeks of gestation. Otherwise, it may be preferable to allow the pregnancy to progress under adequate alpha- and beta-blockade until foetal maturity is reached. Unprepared delivery is associated with a high risk of phaeochromocytoma crisis, characterised by labile blood pressure, tachycardia, fever, myocardial ischaemia, congestive heart failure, and intracerebral bleeding.

Patients with phaeochromocytoma or paraganglioma should be followed up for life. The rate of recurrence is estimated to be 2%–4% at five years [ 10 ]. Assessment for recurrent disease can be accomplished by periodic blood pressure monitoring and 24-hour urine catecholamine and/or metanephrine measurements.

Genetics of Phaeochromocytoma

Approximately one quarter of patients presenting with phaeochromocytoma may carry germline mutations, even in the absence of apparent family history [ 11 ]. The common syndromes of hereditary phaeochromocytoma/paraganglioma are listed in Box 2 . These include Von Hippel-Lindau syndrome, multiple endocrine neoplasia type 2, neurofibromatosis type 1, and succinate dehydrogenase (SDH) gene mutations. Our patient has a novel frameshift mutation in the SDHD gene located at Chromosome 11q. SDH is a mitochondrial enzyme that is involved in oxidative phosphorylation. Characteristically, SDHD mutation is associated with head or neck non-functional paraganglioma, and infrequently, sympathetic paraganglioma or phaeochromocytoma [ 12 ]. Tumours associated with SDHD mutation are rarely malignant, in contrast to those arisen from mutation of the SDHB gene. Like all other syndromes of hereditary phaeochromocytoma, SDHD mutation is transmitted in an autosomal dominant fashion. However, not all carriers of the SDHD mutation develop tumours, and inheritance is further complicated by maternal imprinting in gene expression. While it may not be practical to screen for genetic alterations in all cases of phaeochromocytoma, most authorities advocate genetic screening for patients with positive family history, young age of tumour onset, co-existence with other neoplasms, bilateral phaeochromocytoma, and extra-adrenal paraganglioma. The confirmation of genetic mutation should prompt evaluation of other family members.

Box 2: Hereditary Phaeochromocytoma/Paraganglioma Syndromes

• Von Hippel-Lindau syndrome
• Multiple endocrine neoplasia type 2A and type 2B
• Neurofibromatosis type 1
• Mutation of SDHB , SDHC , SDHD
• Ataxia-telangiectasia
• Tuberous sclerosis
• Sturge-Weber syndrome

Key Learning Points

• Hypertension complicating pregnancy is a commonly encountered medical condition.
• Pre-existing chronic hypertension must be considered in patients with hypertension presenting in pregnancy, particularly if elevation of blood pressure is detected early during pregnancy or if persists post-partum.
• Secondary causes of chronic hypertension include renal artery stenosis, renal parenchyma disease, primary hyperaldosteronism, phaeochromocytoma, Cushing's syndrome, coarctation of the aorta, and obstructive sleep apnoea.
• Phaeochromocytoma presenting during pregnancy is rare but carries high rates of maternal and foetal morbidity and mortality if unrecognised.
• Successful outcomes depend on early disease identification, prompt initiation of alpha- and beta-blockers, carefully planned delivery, and timely resection of the tumour.

Phaeochromocytoma complicating pregnancy is uncommon. Nonetheless, in view of the potential for catastrophic consequences if unrecognised, a high index of suspicion and careful evaluation for secondary causes of hypertension is of utmost importance. Blood pressure should be monitored in the post-partum period and persistence of hypertension must be thoroughly investigated.

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Pregnacy Induced Hypertension (PIH) Case Study

Pregnancy-induced hypertension (PIH) is one of the most common complications of pregnancy. This occurs during the 20 th week of gestation or late in the second trimester of pregnancy. This is a health condition wherein there is a rise in the blood pressure and disappears after the termination of pregnancy or delivery. PIH was formerly called toxaemia or the presence of toxins in the blood. This is because its occurrence was not well understood in the clinical field. Its common manifestations are hypertension, proteinuria (presence of protein in the urine), and edema. There are 2 main types of pregnancy-induced hypertension namely: pre-eclampsia and eclampsia.

• Pre-eclampsia— this is the non-convulsive form of PIH. This affects 7% of all pregnant women. Its incidence is higher in lower socio-economic groups. It may be classified either mild or severe.
• Eclampsia— this is the convulsive form of PIH. It occurs with 5% of all pre-eclampsia cases. The mortality rate among mothers is nearly 20% and fetal mortality is also high due to premature delivery.

NORMAL ANATOMY AND PHYSIOLOGY

There are a lot of bodily changes that happen during a normal pregnancy. There are external changes that are noticeable, and there are internal changes that can only be appreciated through thorough clinical examinations. Most of the changes are the body’s response to the changes in levels of hormones and the growing demands of the fetus.

The two dominant female hormones, estrogen and progesterone , change in a normal level. Along with this, a significant rise/appearance of 4 more major hormones take place; these are 1. human chorionic gonadotropin (HCG), 2. human placental lactogen, 3. prolactin, and 4. oxytocin. All these 6 hormones interact with each other simultaneously to maintain a normal pregnancy as it progresses.

The following are the major effects of these hormones in the body:

The exact cause of pregnancy-induced hypertension is unknown; however, it is highly linked to angiotensin gene T235 and the existence of other risk factors. Malnutrition and inadequate prenatal care are the greatest risk factors. The history and presence of diabetes mellitus (DM), multifetal gestation (twin pregnancies), polyhydramnios (excessive amniotic fluid), and renal diseases are also among the major contributory factors in the development of PIH. In the past, the mystery revolving around PIH postulated a lot of theories on its true origin, most of them were believed to be of toxic nature. Among these are placental infarcts, autointoxication, uremia, pyelonephritis, and maternal sensitization to total proteins.

The i ncidence of PIH among pregnant women is very high (8%), costing hundreds and thousands of lives of both mothers and fetus around the world. This commonly affects first-time pregnancies due to the presence of functioning tropoblasts (develops after the 20 th week of gestation and stays evident until after 48 hours after delivery. Age is also an important indicator in the development of PIH. Too early, as in teenage pregnancies and old primigravidas (first-time pregnancy) as in over 35 years of age put a woman higher chances of having pregnancy-induced hypertension . 

PATHOPHYSIOLOGY

SIGNS AND SYMPTOMS

The signs and symptoms of the type of PIH present in a pregnant woman are based on the presentation of evident clinical manifestations. These are shown in the table below:

COMPLICATIONS

Based on the severity of the PIH present to a person or the extent of damage left/occurred, a list of possible complications can be drawn.

• Abruption placenta
• Disseminated intravascular coagulation (DIC)
• Prematurity
• Intrauterine growth retardation (IUGR)
• HELLP syndrome
• Maternal and/or fetal death  

The changes of the mother and/or fetus to survive after an episode of convulsion or until delivery depends on the threshold on the effects of PIH and its complications. This can be:

• Good— if the symptoms are mild or those that are with mild pre-eclampsia and is responding well to the treatment regimen
•   Poor— if there are multiple and long episodes of convulsions that are associated or lead to the development of persistent coma, hyperthermia, cyanosis, tachycardia, and liver damage.
• Congestive heart failure (CHF)
• Pulmonary edema
• Cerebral hemorrhage
• Renal failure

DIAGNOSTIC EVALUATIONS

            Diagnostic evaluations are performed after episodes of convulsions or after the client has been rushed to a health care facility. These are routinely done to assess the damages and will serve as the basis for the plan of treatment.

• 24-hour urine-protein— health problem through protein determination from the involvement of the renal system.
• Serum BUN and creatinine— to evaluate renal functioning.
• Ophthalmic examination— to assess spasm, papilledema, retinal edema/detachment, and/or hemorrhages.
• Ultrasonography with stress and non- stress test— to evaluate fetal well-being after.
• Stress test —fetalheart tone (FHT) and fetal activity are electronically monitored after oxytocin induction which causes uterine contraction.
• Non-stress test —fetal heart tone (FHT) and fetal activity are electronically monitored during fetal activity (no oxytocin induction).  

NURSING DIAGNOSES

• Fluid volume excess related to altered blood osmolarity and sodium/water retention.
• Altered nutrition, less than body requirements related to loss through damaged renal membrane.
• Altered tissue perfusion related to increased peripheral resistance and vasospasm in renal and cardiovascular system.
• Altered urinary elimination related to hypovolemia.
• Sensory/perceptual alterations: visual related to cerebral edema and decreased oxygenation of the brain.
• Diversional activity deficit related to decreased time for rest and sleep from stimulating environment.
• Risk for injury related to seizure episodes.
• Anxiety-related to fear of the unknown.    

            The overall goal of management in pregnancy-induced hypertension is directed towards the control of hypertension and the correction of developed health problems that might leadto other serious complications. Among the specially-designed treatment course for PIH are the following:

• Use of antihypertensive drugs (hydralazine-drug of choice)
• Diet-high protein, high calories
•   Magnesium sulphate (MgSO4) treatment
• Diazepam and amobarbital sodium (if convulsions don’t respond to MgSO4)
• Beta-adrenergic blockers (used for acute hypertension)
• Delivery (if all treatment regimen don’t work)

NURSING MANAGEMENT

A.   Assessment

•   Monitor blood pressure in sitting or side-lying position.
• Monitor fetal heart tone (FHT) and fetal heart rate (FHR).
• Check for deep tendon reflexes (DTR) and clonus.
•   Monitor intake and output (I&O) and proteinuria.
• Monitor daily weight and edema.
• Assess for signs of labor (possibility of abruption placenta).
• Assess for emotional status.

B.  Interventions

1.  Fluid balance

• Maintain patent and regulated IVF
• Strict I&O monitoring
• Monitor hematocrit level
• Vital signs monitoring every hour
• Assess breath sounds for signs of pulmonary edema

  2.  Tissue perfusion

•  Position on left-lateral position
• Monitor fetal activity (stress and fetal activity)

3.   Preventing injury

• Monitor cerebral signs and symptoms (headache, visual disturbances, and dizziness)
• Lie on left-lateral position if cerebral symptoms are present
• Secure padded side rails
• Keep oxygen suction set, tongue blade, and emergency medications (diazepam and magnesium sulphate) at all times
• Never leave an unstable patient

4.   Anxiety

 Discuss the health condition and planned treatment

• PIH is not lifetime
• PIH is only for the first pregnancy
• All medications and its maternal and fetal effects

Allow to ask questions and answer it truthfully

Provide emotional support to the client and family

C.   Educative

• Reinforce the importance of rest and sleep
• Encourage family cooperation with the treatment course
• Discuss the laboratory procedures and alternative managements
• Include medical team, client, and significant others in the discussion
• Be realistic in discussing the possibilities of premature delivery  
• No sign of pulmonary edema
• Adequate urine output
• No episode of seizure
• Stable and normal heart rate

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Case Study Report on PIH and Severe Pre eclampsia

it is a case study report on PIH and Severe Pre eclampsia I did when I was posted on Kist Medical TEaching Hospital for Midwifery Practicum Prepared by: Rashmi Regmi B Sc Nursing Manmohan Memorial Institute Of health Sciences

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• 1. 1 Prepared by: Rashmi Regmi B. Sc Nursing Manmohan Memorial Institute of Health Sciences OBJECTIVES The main objective of this case study is enabling students to develop knowledge regarding the normal reproductive process, and skill and practice in providing nursing care, provide advices, health teaching to patient and family for management of the disease. During this process I got opportunities to learn about disease condition, its complications and other potential gynecological and obstetric abnormalities and complication that arise due to the disease. General Objectives: To obtain detail obstetric and gynecological history of patient To perform physical assessment of a woman with gynecological and obstetric problem To provide advices, health teaching to patient and family for management of the disease, medications and complications To identify minor and major discomfort and advice the woman relieving measures To apply nursing process to care the client with obstetric and gynecological problems as per her need To identify the different modern technologies to treat the disease for overcoming the problem regarding reproductive health (RH) and educate them about RH.
• 3. 3 PATIENT’s HISTORY 1. Demographic Data Name of Patient: Bimala Gurung Age: 29 years Sex: Female Caste: Gurung Religion: Hindu Marital status: Married No. of Children: 1 Address: permanent: Lumjung Temporary: Harisiddhi, Lalitpur Name of Guardian: Som Gurung (husband) Date Of Admission: 2070/1/19 Inpatient number: 19381 Date of Discharge: Medical Diagnosis: Provisional Diagnosis: G3P2L1 at 26+4 WOG with PIH Final Diagnosis: Pre-eclamsia with HELLP syndrome Economic Status: Medium Occupation: Business 2. Chief Presenting Complaints 1. Epigastric pain X 1-2 hour 2. Vomiting (2 episodes) 3. Headache absent 4. Blurring of vision absent 5. Perceiving good fetal movement 3. History Of Present Illness Past history of Intra Uterine Fetal Death (IUFD) 3 years back at Prasuti Griha, Thapathali due to PIH Sudden onset of severe Epigastric pain accompanied by vomiting, no symptoms perceived earlier
• 4. 4 4. Elaboration Of Patient Chief Complaints In Detail Amenorrhea X 6 months Patient was pregnant with 26+4 weeks of Gestation Patient complained severe heartburn which occurred suddenly before 1-2 hours accompanied by two episodes of vomiting No history of blurring of vision and headache Patient was perceiving good Fetal movement S.N Problem Onset Frequency Severity Alleviating factors Aggravating factors 1. Epigastric pain Sudden (1- 2 hours before) continuous Severe Not relieved by food - 2. Vomiting sudden 2 times Mild - - 5. Obstetric History Married for: 10 years Age of marriage: 16 years Gravida: G3 Parity: P3 Living: 1 a. Abortions (Spontaneous, Induced, Duration Of Pregnancy): Once Induced second Trimester abortion (medical termination of pregnancy) on 2070/1/21 at Kist Medical Teaching Hospital due to PIH complicated by Pre-eclampsia and HELLP syndrome at 26+6 WOG b. Type Of Previous Deliveries (Normal/ Instrumental/ LSCS) Normal vaginal delivery of 1st child (daughter) on 2061/2/26 at Prasuti Griha Thapathali Induced Spontaneous Vaginal Delivery of Second child (son) IUFD 3 years back (2066/4/27) at Thapathali due to IUFD secondary to PIH at 37 WOG
• 5. 5 Third child (daughter) medical termination of pregnancy on 2070/1/21 at Kist Medical Teaching Hospital by spontaneous vaginal delivery as indicated by deteriorating maternal fetal condition due to PIH complicated by Pre-eclampsia and HELLP syndrome at 26+6 WOG c. Significant Antenatal Problem/ 3rd Stage Puerperal Complications In Previous Deliveries: No any significant problem during pregnancy and delivery of first child Antenatal period complicated by PIH on other two pregnancies d. Year And Place Of Previous Deliveries, Sex Of Baby, Living Or Not, If Neonatal Death (Age And Cause Of Death, Congenital Malformation) 2061/2/26 at Prasuti Griha, Thapathali, Female child, living 2066/4/27 at Prasuti Griha, Thapathali, Male child, dead (IUFD) 2070/1/21 at Medical Teaching Hospital, Female child, dead (premature baby) e. Year Of Marriage, Gravida, Para, Abortion, Living Issues No. Year ANC attendance/ pregnancy complication Period of gestation Type of delivery/ abortions Complications in puerperium 1 2061 4 visits/ no any significant complications 37+WOG SVD No any significant complications 2 2066 4 visits/ IUFD due to PIH 37WOG Instrumental delivery (Forcep delivery) No any significant complications 3 2070 2 visits / MTP due to PIH 26+WOG SVD No any significant complications Age of last child birth/ year of last pregnancy: 3 years, 2066/4/27
• 6. 6 6. Menstrual History Age of menarche: 14 years Duration of flow: 6-7 days Length of cycle (from 1st day of one cycle to 1st day of next cycle): 30 days Regular/ irregular (range of shortest – longest cycle) : 28- 30 days Amount of flow, passage of clots, no. of soaked pads/ day : normal, passage of some clots, 2pads/day Dysmenorrhea (severity, duration): No history of dysmenorrhea Intermenstrual bleeding: Absent Post coital bleeding: Absent Last menstrual period (LMP): 2069/7/15 7. Contraceptive History Type of contraception, duration, cause of discontinuation: Oral Contraceptive Pills, 3 years, for conception 8. Past History: Pregnancy Induced Hypertension 3 years back 9. Medical History Immunization: Done Allergies (food, drug, environment): Absent Previous hospitalizations ( if yes reasons): 22 days on 2nd pregnancy due PIH on third trimester Injuries/ accidents: Not any
• 7. 7 10. Chronic Illness SN Diseases In patient In family Yes No Yes No 1 Hypertension Yes No 2 Cardiovascular diseases No No 3 Diabetes No No 4 Tuberculosis No No 5 Asthma No No 6 Cancer No No 7 Malaria No No 8 Filarial No No 9 Others No No 11. Surgical History Surgeries/ operations (minor/ major), year, type, indication: Not Any 12. Treatment History Any treatment done for present illness or any medication which patient is taking regularly? Not Any Traditional healer prescription: Not Any Medical practitioner’s prescription: treated for gestational hypertension on last pregnancy 3 years back but as symptom subsided after delivery and blood pressure returned to normal no any treatment continued at home Self prescription: Not Any 13. Personal History Smoking: Absent Alcohol intake: Absent Rest and sleep: adequate rest and sleep Recreation habit: watching television Elimination: normal bowel and bladder habit Hygiene: hygienic
• 8. 8 Dietary habits: balanced diet supplemented by extra sources of vitamins, minerals and proteins like meat, milk, fruits and vegetables 14. Miscellaneous a. For Antenatal Cases: Duration of cessation of menses: approximately 4 months LMP: 2069/7/15 EDD: 2070/4/22 Gestation in weeks (by date): 26+4 WOG Fetal movements: date of perception and whether normal or not: date of perception not known, around 16 WOG, perceiving normal fetal movements ANC attendance (place, regularity and starting): Regular, Health post Harisiddhi starting 1st trimester TT immunization: Once Taking iron/calcium or any other drugs: under regular Iron and Calcium supplementation b. Any Problems In Each Trimester (e.g. severe vomiting, pain abdomen, fever, urinary problems, vaginal bleeding or abnormal discharge, severe headache, swelling, any conditions requiring hospital admissions during this pregnancy) Second Trimester presented with Severe Epigastric Pain and vomiting, and generalized edema 15. Family History Tuberculosis, diabetes mellitus, hypertension, female genital tract malignancies: Absent In antenatal cases: multiple pregnancies, congenital malignancies (esp. Down ’s syndrome): Absent
• 9. 9 16. Family tree 87 years 64yrs 92yrs (Unknown) 82yrs alive (fall injury) 68 yrs 66yrs 63yrs 58yrs 56yrs 52yrs 50yrs 60yrs 57yrs 54yrs 50yrs 48 34yrs 33yrs 29yrs 27yrs 24yrs Healthy Healthy PIH Healthy Healthy Key: Alive healthy male Alive healthy female Patient Dead male Dead female P P
• 10. 10 PHYSICAL EXAMINATION FINDINGS Examination Findings A. General examination INSPECTION 1. Observe client’s ability to respond to verbal commands The client is confused and disoriented, inappropriate responses 2. Observe client’s LOC (level of consciousness) Lowered LOC 3. Observe facial expression and mood Eyes are closed Client was frowning Client was unable to answer questions 4. Observe general appearance; posture, gait, movement Patient needed support to stand and walk Decreased movement Even gait 5. General state of health Weak appearance 6. Nutritional status Well nourished 7. Behavior Inappropriate reaction to situation, disoriented 8. Responses Not responding well 9. Cleanliness Hygiene maintained but not well groomed 10. Speech Clear, adequate pace VITALS Temperature: 97º f Pulse Rate: 82/min Blood Pressure: 140/110 and 150/110 in right and left hand Respiratory Rate: 20/min Height : 156cm Weight: 56kg Normal temperature Normal pulse rate Hypertension (high blood pressure) Normal respiratory rate B. Skin Assessment INSPECTION AND PALPATION 1. Inspect skin from head to toe Slightly pale and yellowish skin color Erythema present on skin of hip 2. Palpate skin for moisture and texture Slightly moist, no excessive moisture or dryness Firm, smooth, soft, elastic skin 3. Palpate skin for temperature Warmth 4. Palpate skin for hydration and turgor Pinched skin promptly returns to it’s
• 11. 11 previous state when released No sign of dehydration 5. Press suspected edematous areas with the edge of the finger for 10 seconds and observe for the depression Presence of pitting edema in ankle 6. Inspect skin for lesions, cut and surgical incision Skin is intact No variation in pigmentation and texture Freckles, moles and warts are normal C. Nail 1. Inspect and palpate the fingernails and toenails note color, shape and any lesion Pink colour 2. Check capillary refill by pressing the nail edge to blanch and then release pressure quickly, noting the return of color Normal return of color <3 sec No discoloration, ridges, pitting, thickening or separation from the edge D. Hair and Scalp 1. Inspect hair for color, texture, growth, distribution Color Black, fine texture, wavy hair 2. Inspect scales, lumps, nevi or other lesions No lumps, lesions, scales and nevi E. Head 1. Observe the skull for size, shape and symmetry Skull symmetrical, round and erect on midline 2. Palpate skull for deformities, depression, lump or tenderness No depression, lumps, tenderness and any deformities F. Face 1. Inspect for abnormal facial expression, gestures and involuntary movements, swelling and masses Normal facial expression No any involuntary movements Swelled face 2. Palpate face for edema, tenderness and depression Peri- orbital edema present around eyes G. Sinuses 1. Palpate sinuses for tenderness No tenderness in frontal, maxillary and ethmoid sinuses H. Eye 1. Inspect both eyes for position and alignment No deviation from normal condition 2. Eye brows inspected for distribution and any scaliness Uniform distribution and no scaliness
• 12. 12 3. Eyelashes inspected for infection and sty No infection or sty 4. Conjunctiva inspected for redness, paleness, discharge, foreign body, dryness or tearing No redness, paleness, discharge, foreign body, dryness or tearing 5. Inspect sclera for color change, injury and dilated blood vessels Slightly yellowish sclera 6. Cornea for color, abrasion and white spots Transparent , no abrasion or white spots 7. Pupil for size, shape and symmetry comparison Pupil round, symmetrical and uniform 8. Co-ordination of eye movement Good eye movement and co- ordination 9. Papillary reaction to light Normal papillary 10. Lens inspected for opacity Lens transparent 11. Convergence test Normal (positive) I. Ear 1. Location and size The top of pinna cross the occiput line Equal size bilaterally 2. Pinna for any lump or lesion No lump or lesion 3. The external auditory canal for ear discharge, mass foreign body and crumen No discharge, redness, masses or foreign body, small amount of crumen present 4. Palpate for tenderness No pain while moving pinna or palpating mastoid process 5. Weber test Sound heard equally on both ear 6. Rinne Test Air conduction of sound is greater than bone conduction J. Nose 1. Location of nose Centrally located 2. Nostrils for their size and symmetry Uniform in size and symmetrical 3. Nasal septum for polyp No polyp 4. Nasal canal Pink mucosa, no discharge or foreign body K. Mouth And Throat 1. Lip for color, moisture, cracks or ulcer Lip pink in color, moist, no discoloration, cracks or ulcer
• 13. 13 2. The mucous membrane of the mouth for color, ulcer, nodules and amount of saliva Pink, moist, mucous membrane, no ulcer, nodules, adequate saliva 3. Gum for inflammation, swelling, redness and bleeding Pink gum, no inflammation, swelling, redness and bleeding present 4. Teeth for color, cavities and missing teeth White color, No missing teeth, cavities present 5. Tongue for symmetry, color and papillae Pink, moist, symmetrical, papillae normal 6. Pharynx and tonsils observed No inflammation and swelling and difficulty swelling L. Neck INSPECTION a. Ask patient to sit straight No tilting of neck b. Observe for masses, congenital goiters, scars, distended jugular vein No masses, congenital goiters, scars or distended jugular vein c. Thyroid gland No enlargement of thyroid gland d. Ability to move neck No neck stiffness, smooth range of motion and no tenderness Palpation 1. Thyroid gland palpated to exclude goiter, masses and enlargement No goiter, , masses and enlargement 2. The back of neck along the spine and back No abnormal alignment of spine M. Lymph nodes 1. Inspection and palpation of lymph nodes for enlargement and tenderness No tenderness or enlargement N. Chest and lungs INSPECTION 1. Shape, size and symmetry Lateral diameter wider than antero posterior diameter Symmetrical, sternum located at midline 2. Bilateral expansion of lungs Equal expansion of both lungs PALPATION 1. Chest for expansion, lumps, tenderness and depression along ribs Equal Bilateral expansion of lungs, no lumps, tenderness or depression noted
• 14. 14 PECUSSION 1. The front and back of chest from apex to base Resonant sound heard over the entire chest, anteriorly and posteriorly AUSCULTATION 1. The front and back of the chest to evaluate breath sound using stethoscope Vesicular sound heard all over the lungs 2. Compare duration of inspiration and expiation Inspiration longer than expiration 3. Check for abnormal breathe sound like rales, fine crackles, rhonchi and wheezing No rales, rhonchi or wheezes present Breathing sound clear O. Heart INSPECTION 1. Enlargement of neck veins No enlargement of jugular veins AUSCULTATION 1. Aortic area (2nd intercostals space just right of the sternum) 2. Pulmonic area (2nd intercostals space just left of the sternum) 3. Tricuspid area (5th intercostals space just left of the sternum) 4. Mitral area (5th intercostals space at midclavicular line) Clear regular heart rate 84/min No abnormal S3 heart sound present 5. Note the clarity and regularity of heart sound Regular, Normal heart sound S1 and S2 present No abnormal heat sound like gallop and murmur present P. Female Breast INSPECTION 1. Size and shape of the breast, observe nipple condition Breasts and nipples are uniform in shape and size, nipples are pointed in same direction Left breast slightly larger than right breast 2. Look for swelling, dimpling or retraction of breast No swelling, dimpling or retraction of breast 3. Nipples for cracks and discharge No cracks and discharge PALPATION 1. Both breast were palpated in circular motion for masses, swelling Soft, non tender, no masses, lumps and swelling were detected
• 15. 15 Q. Abdomen INSPECTION 1. For shape, size, dilated veins, straie, previous incisional scars, lesions Round shape, no distention, lesions, previous incisional scars or dilated abdominal veins present Linea nigra and striae gravidarum present AUSCULTATION 1. For bowel sound (increased bowel sound or decreased bowel sound by placing stethoscope for 5 minutes) 2. Note type of sound Bowel sound present in all areas in every 20 seconds Gurgling sound present PECUSSION 1. Keep patient in supine position and percuss abdomen in all four quadrants Tympanic sounds heard over gas- filled viscera and dull sound over fluid filled viscera Dull sounds were more prominent PALPATION 1. Keep patient in supine position and ask patient to relax abdomen, palpate abdomen in all 9 parts Feel for any masses and tenderness No abdominal masses and tenderness 2. Palpate liver, place left hand on 11th and 12th rib and apply firm pressure to push liver forward towards the right hand Note enlargement and tenderness Liver not palpable, no tenderness or enlargement 3. Spleen: keep patient in right lateral position, place left hand on patient’s back under the left rib cage Spleen not palpable, no enlargement or tenderness 4. Kidneys: keep patient in supine position, place left hand on the on patient’s back between the lowest rib and the pelvic bone. Ask patient to take deep breath, press firmly with right hand and try to palpate kidney. Repeat same process for left side too Note enlargement and tenderness Kidneys non palpable and non tender R. Anus INSPECTION 1. Anus for irritation, hemorrhoids, cracks, fissure No irritation, hemorrhoids, cracks, fissure
• 16. 16 S. Genital Area INSPECTION 1. Vulval swelling, discharge, condition of perineum, labia for color, redness, swelling of labia No discoloration, swelling, or redness No abnormal vaginal discharge 2. Check for urethral orifice for redness or discharge No redness or discharge 3. Vaginal discharge or bleeding from vagina No abnormal Vaginal discharge or bleeding from vagina T. Musculoskeletal System INSPECTION 1. The muscles and joints ask patient to perform range of motion exercises, joint movement of neck, wrist, ankle, hip in all possible direction Patient was unable to perform ROM exercises due to patients deteriorating condition and generalized body pain Patient was in no condition to perform it 2. Patient’s supine, note placement and curvature Spine is in midline;slightly curved out from neck inward at the waist PALPATION 1. Palpate joints for swelling, tenderness and temperature No joint swelling, or tenderness, normal temperature 2. Ask patient to perform range of motion exercises, joint movement of neck, wrist, ankle, hip in all possible direction Patient was in no condition to perform it U. Nervous System 1. Muscle strength, push against patient’s hand and ask to resist push Weak muscle strength 2. Sensation Present 3. co-ordination of movements co-ordinated motor activities V. Reflexes 1. Biceps reflex Contraction of the biceps muscle and flexion of the forearm 2. Triceps reflex Normal response, extension of forearm 3. Knee jerk Extension of lower leg 4. Plantar reflex Flexion of all toes and inversion and flexion of the forefoot
• 17. 17 SUMMARY OF FINDINGS Physical examination was performed from head to toe OF Mrs. Bimala Gurung, 29 years female with diagnosis of PIH with severe pre-eclampsia on 2070/1/19. The findings obtained are listed below Weight: 156cm Height: 56kg Vital Signs Temperature: 97º f Pulse: 82/m Respiration: 20/m Blood Pressure: 140/110mm Hg and 150/110 mm Hg Findings: General Appearance: weak appearance Gait: Imbalanced Nutritional Status: well built Facial Expression: frowning Skin: pale and yellowish Bilateral pedal edema present, Peri- orbital edema present around eyes Head: normal contour, no lesions were observed Chest: no added murmur sounds were heard, no adventitious breathe sound heard Abdomen: no organomegaly (hepatomegaly/ spleenomegaly), no dilated veins over abdomen, straie gravidarum and linea nigra present, no masses and tenderness over abdomen present Genitalia: No discoloration, swelling, or redness, No abnormal vaginal discharge present Musculoskeletal: weak muscle strength Reflexes: normal reflexes
• 18. 18 DEVELOPMENTAL NEED AND TASK As my patient is 29 years old female, she is at young adulthood stage (18-35years) in her life. According to book According to Diekelmann (1976) there are five developmental task of young adulthood and they are: The young adult achieve independence from parental control They begin to develop strong friendships and intimate relationship outside the family They establish personal set of values They develop a sense of personal identity They prepare for life work and develop the capacity for intimacy In my patient She achieved independence from parental control She formed an intimate relationship with her husband She has her own set of personal values She has developed a sense of personal identity She has prepared herself for life and has already built the capacity for intimacy
• 20. 20 HYPERTENSIVE DISORDERS IN PREGNANCY Introduction Hypertensive disorders in Pregnancy is regarded as one of the most serious medical disorders in pregnancy It may complicate 5-15% of all pregnancies and is responsible for 15-20% of all maternal mortality in developing and developed countries There is a generalized vasospasm leading to systemic disorders involving the vital organs of the body. Hence, any vital organ failure can lead to chronic illness Classification of Hypertensive Disorders In Pregnancy 1. Gestational Hypertension or Pregnancy Induced Hypertension or Transient Hypertension 2. Pre-eclampsia 3. Eclampsia 4. Superimposed Pre-eclampsia 5. Chronic Hypertension Chronic Hypertension may be associated with: Essential Hypertension Chronic Renal Diseases Co-arctation of Aorta Pheochromocytoma Thyrotoxicosis (hyperthyroidism) Connective Tissue Disease Systemic Lupus Erythematous
• 21. 21 Definitions 1. Normal Blood Pressure Normal Blood Pressure normally falls in pregnancy with no change in systolic blood pressure but diastolic blood pressure is lowered by 10 mmHg with lowest recording at 14-20 weeks of pregnancy, before rising to pre-pregnancy value by term the mid trimester fall in blood pressure is due to significant decrease in vascular tone following the cardiovascular alterations leading to peripheral vasodilation 2. Gestational Hypertension It is a condition in which systolic blood pressure is greater than 140mmHg and diastolic blood pressure is greater than 90 mmHg or more on at least two occasions four or more hours apart beyond 20th weeks of gestation or during 24 hours after deliver in previously normotensive woman 3. Pre-eclampsia Pre-eclampsia is Pregnancy Induced Hypertension in association with significant Proteinuria 4. Eclampsia Eclampsia is defined as seizures that cannot be attributed to any other cause in women with pre-eclamsia 5. Chronic hypertension Chronic Hypertension is hypertension antedating pregnancy or hypertension diagnosed before 20 weeks of pregnancy but not attributable to gestational trophoblastic disease It is also known hypertension before pregnancy or hypertension. Diagnosed in first trimester before 20 weeks of pregnancy and persisting 12 weeks of postpartum is also considered as chronic hypertension
• 22. 22 6. Super-imposed Pre-eclampsia It is the development of pre-eclampsia in a patient with chronic hypertensive vascular or renal disease when hypertension antedates the pregnancy as established by previous blood pressure recordings. Criteria A rise in systolic blood pressure by 30 mmHg or A rise in diastolic blood pressure by 15 mmHg and Development of proteinuria or edema or both Above criteria should be fulfilled during pregnancy to establish the diagnosis of Super-imposed Pre-eclampsia PREGNANCY INDUCED HYPERTENSION It is a condition in which systolic blood pressure is greater than 140mmHg and diastolic blood pressure is greater than 90 mmHg or more on at least two occasions four or more hours apart beyond 20th weeks of gestation or during 24 hours after deliver in previously normotensive woman Criteria for diagnosis of Pregnancy Induced Hypertension Absence of any evidence for underlying causes of Hypertension Unassociated with other evidences for pre-eclampsia (edema or proteinuria) Not associated with haemoconcentration,, thrombocytopenia, raised serum uric acid level and hepatic dysfunction
• 23. 23 PRE-ECLAMPSIA Pre-Eclampsia is a multisystem disorder of unknown etiology characterized by development of hypertension to the extent of 140/90 mmHg or more with proteinuria after the 20th week of pregnancy in previously normotensive and non proteinuric patient. Some amount of edema is common in normal pregnancy thus edema has been excluded from diagnostic criteria unless it is pathological. The pre-eclamptic features may appear before 20th week of pregnancy as in case of H.mole and polyhydraminous Pre-Eclampsia is disease of unknown etiology occurring after 20th week of gestation characterized by blood pressure more than 140/90mmHg (systolic blood pressure >30mmHg and diastolic blood pressure >15mmHg) over previously documented blood pressure and mean arterial pressure > 105 or >20mmHg over previously documented Mean arterial pressure with significant proteinuria (>0.3g/ 24hours) and generalized edema Criteria Pre-eclampsia is diagnosed when a pregnant woman develops both: Blood Pressure >140 systolic and/or >90 diastolic (two separate readings taken at least six hours apart) 300 mg of protein in a 24-hour urine sample (proteinuria). INCIDENCE 5-15% of all pregnancies, more common in primigravida and is about 10% and 5% in multigravida Increasing incidence in developing countries and if unrecognized, it is the most serious life threatening condition to both mother and fetus
• 24. 24 RISK FACTORS Genetic factors Family history: (hypertension, pre-eclampsia, eclampsia) Genetic disorder Obstetric factors Primigravida: young or elderly (first time exposure to chorionic villi, <20/>40 years) Obstetric complications e.g. H.mole, twins, diabetes Rh incompatibility Previous history of pre-eclampsia Placental abnormalities: i. hyperplacentosis: excessive exposure to chorionic villi- (molar pregnancy twins, diabetes) ii. placental ischaemia iii. hydrops fetalis with large placenta iv. poor placentation New paternity Medical factors Obesity: BMI>35kg/M², insulin resistance Pre-existing vascular disease or renal disease Thrombophilias (antiphospholipid syndrome, protein C,S deficiency, Factor V leiden) Immunological phenomenon Chronic hypertension Diabetes Connective tissue diseases like SLE Hyperhomocystinaemia Polycystic ovarian disease
• 25. 25 ETIOPATHOLOGICAL FACTORS FOR PRE-ECLAMSIA 1. Failure of trophoblastic invasion 2. Vascular endothelial damage 3. Inflammatory mediators 4. Immunological intolerance between maternal and fetal tissues 5. Coagulation abnormalities 6. Increased oxygen free radicals 7. Genetic predisposition (polygenic disorder) 8. Dietary deficiency of excess ETIOPATHOGENESIS OF PRE-ECLAMPSIA Pre-eclampsia has been described as a disease of theories, because the cause is unknown. Some theories include Endothelial cell injury, Immunological phenomenon (insufficient production of blocking antibodies), Placental pathology Altered vascular reactivity, Imbalance between prostacyclin and thromboxane, Decreased glomerular filtration rate with retention of salt and water, Decreased intravascular volume, Increased central nervous system irritability, Disseminated intravascular coagulation, Uterine muscle ischemia Dietary factors, and Genetic factors.
• 26. 26 1. Placental Pathology: pre-eclampsia and idiopathic IUGR are part of the same disease spectrum and both are primarily due to abnormal placentation. In normal pregnancy, the spiral arteies of placenta are invaded by the cytotroblast and the elastic and muscular coats are replaced by fibroid tissues. Early in second Trimester, a second wave of cytotrophoblast invasion transforms the myometrial segments of the spiral arteries into wide mouthed vessels unresponsive to vasomotor stimuli. Thus, the blood supply is transformed from a high resistance low flow system to a low resistance high flow system in order to increase the uteroplacental flow and meet the needs of fetus In pre-eclampsia, the primary wave of trophoblastic invasion partly impaired and the second wave fails to occur. This results in reduced uteroplacental flow which worsens as gestation advances. In addition, the arteries remain very sensitive to vasomotor stimuli. These changes are not specific to Pre-eclampsia and can occur in IUGR without pre-eclampsia. 2. Endothelial Cell Dysfunction and Vasospasm It is the primary pathology of pre-eclampsia. The precise mechanism by which the ischaemic placenta causes widespread endothelial cell damage in preeclampsia is not known. one theory is that it is caused by lipid perioxidation stimulated by free oxygen radical because of oxidative stress. Prostacyclin is a prostaglandin produced by vascular endothelium and is a powerful vasodilator and inhibitor of platelet aggregation. Nitric oxide is another vasodilator produced by the endothelium. Thromboxane is produced by the platelets and causes vasoconstriction and platelet aggregation. In normal pregnancy, there is an increase in prostacyclin resulting in vasodilation In pre-eclampsia, due to the endothelial cell dysfunction between prostacyclin anion there is a reduction in prostacyclin and nitric oxide, so overall, there is a shift in the balance between prostacyclin and thromboxane in favors of thromboxane. Therefore, there is vasospasm, platelet activation and activation of coagulation system. Apart from this, in normal pregnancy the peripheral resistance and thus blood pressure, falls due to the acquired insensitivity to the pressor effect of angiotensin II. In contrast, in pre-eclampsia there is loss of vascular
• 27. 27 insensitivity. This results in vasospasm and thereby an increase in vascular resistance and increase in blood pressur 3. Coagulation system and platelets Endothelial dysfunction will lead to activation of platelets and coagulation system by the tissue factor on the endothelium. This results in widespread DIC and hence platelets and clotting factors are used up. The disturbance may range from subclinical to pathological DIC. These results in consumption of clotting factors and platelets may manifest thrombocytopenia. Tissue factors is increased in pre-eclampsia and stimulated by cytokines like Tumor Necrosis Factor (TNF). So, activation of the coagulation system is also linked to pro-inflammatory state. As a result of all these changes there are widespread multiple small hemorrhages and fibrin deposition in many organs. 4. Metabolic factors central obesity and insulin resistance are risk factors for pre-eclampsia. There is a dramatic increase in free fatty acids and triglycerides in pre-eclampsia, which may be due to the insulin resistance. The hyperlipidaemia may induce endothelial dysfunction directly. Alternatively, oxidative stress can result in free oxygen radicals producing lipid perioxidation, which can also result in endothelial dysfunction. Therefore, pre-eclampsia may be the pregnancy as associated expression of the metabolic syndrome. 5. Genotype and phenotype There is definitely an inherited maternal component in pre-eclampsia. The placenta is probably the trigger, but it is the maternal response that is critical. We know that there is a familial tendency. The same problem of abnormal placentation causes both pre-eclampsia and idiopathic IUGR. Hence, it is possibly those women who do not have susceptible genotype or phenotype, which develop IUGR without pre-eclampsia.
• 28. 28 PATHOPHYSIOLOGY Primary cause unknown (genetic/ immunological) Initial phase: vascular pathology Failure of second wave of trophoblast invasion Decrease blood flow in spiral artery Decrease placental blood flow Placental bed ischemia Stimulation of macrophage system Liberation of TNF α (trigger) interleukins oxygen free radicals lipid peroxides Endothelial damage/ dysfunction
• 29. 29 a. Placenta: the placental changes are central to pre-eclampsia. The typical vascular lesion is termed as acute atherosis. This is characterized by fibrinoid necrosis, macrophages and mononuclear cell infiltration b. Kidney: the main pathology of kidney is glomerular endotheliosis which narrows lumen. This comprises swollen endothelial cells due to fibrin deposition. There is glomerular and tubular dysfunction. The main pathology is glomerular dysfunction, the manifestation of which is proteinuria. There is also a reduction in the glomerular filtration rate and creatinine clearance, which in severe cases leads to an increase in the blood urea and serum creatinine. Acute renal failure can rarely supervene and is usually due to acute tubular necrosis which is reversible. Very rarely, it is due to irreversible acute cortical necrosis tubular dysfunction is manifested as hyperuricaemia. c. Liver: Periportal thrombosis and fibrin deposition, hemorrhages and necrosis seen in the liver. There is an increase in the liver enzymes SGOT and SGPT and clinical jaundice can occur. The liver changes are responsible for the nausea and vomiting in severe cases. The small hemorrhages may coalesce to form a sub capsular hematoma, which may cause stretching of the Gilson’s capsule and Epigastric pain. This is a very serious sign and seen in impending eclampsia. These changes are responsible for HELLP syndrome, which is described as an extremely rare but catastrophic complication and may lead to liver rupture. d. Brain: The main finding in brain is the cerebral vasospasm. Small cerebral hemorrhages, thrombosis and fibrinoid necrosis can occur especially in eclampsia and are secondary to endothelial dysfunction. Cerebral edema is also usual in eclampsia. Massive cerebral haemorrhages are a rare complication of severe hypertension. Visual disturbances are common and are usually due to edema of the occipital lobe. Cortical blindness can rarely occur due to occipital edema which is usually temporary. e. Eyes: localized retinal vasospasm is the commonest finding. Hemorrhages and papilloedema may be seen rarely in severe hypertension. Blindness could rarely be due to retinal artery ischemia or infraction. Another complication is retinal detachment, which usually improves with time.
• 30. 30 CLINICAL TYPES The clinical classification of Pre-eclampsia is principally dependent on the level of the blood pressure. It is classified into a. Mild Pre-eclampsia b.Severe Pre-eclampsia a. Mild Pre-eclampsia: It includes cases of sustained rise of blood pressure of more than 140/90 mmHg but less than 160mmHg systolic or diastolic without significant proteinuria. b. Severe Pre-eclampsia: It comprises of A persistent systolic blood pressure of ≥160mmHg or diastolic pressure of >100mmHg Proteinuria excretion of >5gm/24hrs Oliguria (<400ml/24hr) Platelet count <100,000/mm³ HELLP syndrome Cerebral or visual disturbances Persistent severe Epigastric pain Retinal hemorrhages, exudates or papilloedema Intrauterine growth restriction of the fetus Pulmonary edema
• 31. 31 Indicators of mild to moderate and severe preeclampsia Site Indicator Mild to Moderate Severe Central nervous system Symptoms and signs Hyperreflexia Headache Blurred vision Headache Irritability Kidney Proteinuria 0.3-5 g/24 h > 5 g/24 h or catheterized urine with 4+ protein Urinary output > 20-30 mL/h < 20-30 mL/h Liver AST, ALT, LDH Normal Elevated LFTs Epigastric pain Ruptured liver Hematologic Platelets Hemoglobin > 100,000/uL Normal range < 100,000/uL Elevated Vascular Blood pressure < 160/110 mm Hg >160/110 mm Hg Retina Arteriolar spasm Retinal hemorrhages Fetal- placental unit Growth retardation Absent Present Oligohydramnios Fetal distress May be present Absent Present Present Key: AST = aspartate aminotransferase; ALT = alanine aminotransferase; LDH = lactate dehydrogenase; LFTs = liver function tests.  My patient was presented with severe Pre-eclampsia.
• 32. 32 ECLAMPSIA Eclampsia is an acute and life-threatening complication of pregnancy, characterized by the appearance of tonic–clonic seizures, usually in a patient who has developed pre-eclampsia. Eclampsia includes seizures and coma that happen during pregnancy but are not due to preexisting or organic brain disorders Sign and Symptoms - Patients show signs of pregnancy-induced hypertension and proteinuria before the onset of the eclamptic convulsion. - Other cerebral signs may precede the convulsion such as nausea, vomiting, headaches, and cortical blindness - With the advancement of the pathophysiological process, other organ symptoms may be present including abdominal pain, liver failure, signs of the HELLP syndrome, pulmonary edema, and Oliguria - The fetus may be compromised by intrauterine growth retardation, and with the toxemic changes during eclampsia may suffer fetal distress - Placental bleeding and placental abruption may occur. Seizures It is divided into following 4 stages: 1. The stage of invasion facial twitching can be observed around the mouth. 2. The stage of contraction tonic contractions, or sustained muscular contractions without intervals of relaxation, render the body rigid; this stage may last about 15 to 20 seconds. (Tonic contractions are also known as tetanic contractions). 3. The stage of convulsion when involuntary and forceful muscular movements occur, the tongue may be bitten, foam appears at the mouth. The patient stops breathing and becomes cyanotic; this stage lasts about one minute. 4. Coma. When the patient awakens, she is unlikely to remember the event. In some rare cases there are no convulsions and the patient falls directly into a coma. Some patients may experience temporary blindness upon waking from the coma.
• 33. 33 CLINICAL FEATURES According To Book In My Patient Onset Usually insidious onset but on rare occasions onset may be acute and rapid Onset acute and rapid Symptoms Mild symptoms Slight swelling over ankles which persists on rising from bed in morning and tightness of the ring finger Swelling over ankles present Swelling gradually extending to face, body, abdominal wall, vulva and whole body Generalized edema present with peri-orbital edema around eyes and face Alarming symptoms (usually associated with acute onset) Headache – either located in occipital or frontal region Headache present Disturbed sleep pattern Absent Diminished urinary output – urinary output less than 400ml in 24 hours Diminished urinary output present Epigastric pain- acute pain in the Epigastric region associated with vomiting, coffee color vomitus due to sub capsular haemorrhage in the liver Acute Epigastric pain with vomiting
• 34. 34 Eye symptoms- blurring, scotomata, dimness of vision or at times complete blindness vision regained within 4-6 weeks Blurring of eye initially absent but present as disease progressed Signs Abnormal Weight Gain- within short span of time. A rapid weight gain of more than 5lbs or more than 1lbs a week Absent Rise of blood pressure: the rise of blood pressure may be insidious or abrupt. Diastolic pressure rises followed by systolic pressure Present blood pressure raised up to 160/120 mm Hg Edema: visible edema over the ankles on rising from bed in morning, generalized edema in severe cases. Generalized edema present No manifestation of chronic cardiovascular and renal pathology No manifestation of chronic cardiovascular and renal pathology Pulmonary edema: due to leaky capillaries and low oncotic pressure Absent Abdominal examination: reveals evidences of chronic placental insufficiency such as Oligohydramnios, IUGR Absent, IUFD occurred due to induction of labour
• 35. 35 INVESTIGATIONS According to Book In my Patient Blood Pressure measurement ✓ CBC (Hb, TC, DC, ESR) ✓ Blood Grouping and Cross Matching ✓ Coagulation Profile (PT, CT, BT, APPT) ✓ Hematocrit ✓ Liver Function Test: Serum Alanine Aminotransferase (ALT) Aspartate Aminotransferase (AST) levels Indirect Bilirubin ✓ Renal Function Test: Serum creatinine BUN Creatinine Clearance Creatinine urine ✓ 24-hour urine collection for protein Urine Dipstick Test ✓ Urine analysis ✓ Peripheral blood smear ✓ Serum lactate dehydrogenase (LDH) level X Ultrasonography: Trans abdominal, to assess the status of the fetus and evaluate for growth restriction; umbilical artery Doppler ultrasonography, to assess blood flow ✓ Fundoscopy ✓
• 36. 36 INVESTIGATIONS RESULTS Investigations Findings in my patient Normal values Blood Pressure 160/110 – 150/90mmHg 120/80 mmHg TLC DLC: Neutrophils Lymphocytes Eosinophils HB Platelets 12,800/mm³ 60 38 02 9mg/dl 86,000/cumm 4,000-12,000 54-62% 25-30% 1-3% 12-15mg/dl 1,50,000-4,50,000/cumm Blood Grouping and cross matching A Negative Coagulation Profile: BT- CT- INR- 10min 14min 9.0 1-6min 1-10min 0.8-1.2 Biochemistry: Urea Creatinine Sodium Potassium Bilirubin total Bilirubin direct SGOT (AST) SGPT (ALT) Total Protein Albumin LDH RBS Uric Acid 25mg/dl 1.1mg/dl 142mmol/l 2.9mmol/dl 4.76 mg/dl 3.2 mg/dl 1837U/L 913U/L 7.2 gm/dl 4.8 gm/dl 2057IU/L 83mg/dl 4.7mg/dl 10-40mg/dl 0.4-1.4mg/dl 135-146mmol/L 3.5-5.2mmol/L Up to 1.0mg/dl Up to 0.2mg/dl 0-40U/L 0-40U/L 6-8gm/dl 3.5-5.5gm/dl <480 IU/L Up to 140mg/dl 2.4-5.7mg/dl Urinalysis: Reaction: alkaline Colour: yellow Epi cells: 16-18/hpf RBC: 10-12/hpf WBC: 14-16/hpf Albumin: 3+ 24 hour urine Protein Positive Fundoscopy No retinal detachment seen USG Singleton preganancy of 25 WOG
• 37. 37 COMPLICATIONS Complications can be classified as immediate and remote Immediate: 1. Maternal During pregnancy: a. Eclampsia b. Accidental hemorrhages c. Dimness of vision and even blindness d. Preterm Labour e. HELLP syndrome f. Oliguria and Anuria g. Cerebral Hemorrhages h. Acute Respiratory Distress Syndromes (ARDS) i. Disseminated intravascular coagulation (DIC) j. Acute fatty liver of pregnancy k. Acute renal failure l. Placental abruption During labour a. Eclampsia b. Postpartum hemorrhages- related with coagulation failure Puerperium a. Eclampsia- usually occurs within 48 hours b. Shock- Puerperal vasomotor collapse c. Sepsis 2. Fetal The fetal risk is related to the severity of the pre-eclampsia Prematurity Intrauterine growth retardation (IUGR) Intrauterine Fetal Death (IUFD)
• 38. 38 MANAGEMENT Mild Pre-eclampsia Mild pre-eclampsia can be managed in OPD basis, especially those without proteinuria. Monitoring maternal and fetal condition is essential. Bed rest in left lateral position is suggested. No sedatives, salt restrictions and diuretics are suggested as they further reduce uteroplacental flow and worsen IUGR, the only indication of diuretics is pulmonary edema Anti-hypertensives The effect of anti hypertensive in Mild pre-eclampsia is controversial. It is prescribed only when diastolic blood pressure is more than 100 mm Hg and systolic blood pressure is more than 160 mm Hg. The main objective is to reduce the risk of severe hypertension and cerebral hemorrhage, once the Mean Arterial Pressure is more than 150, there is loss of cerebral auto regulation and high risk of cerebral hemorrhage. The use of anti hypertensive may help in prolongation of pregnancy. The drug of choice in pregnancy is α-methyldopa. Other commonly used first line drugs are nifedipine and labetalol. labetalol should be avoided in woman with known asthma. Beta blockers like Atenolol can cause IUGR and thus avoided. ACE inhibitors are absolutely contraindicated in Pregnancy as they can impair renal function causing fetal Oliguria and oligohydraminous. Blood pressure and urine albumin daily Twice weekly Peripheral Blood Smear, platelet count, coagulation profile, uric acid, renal and liver functions tests Fetal Daily fetal movement count Ultrasound to assess fetal growth and well-being NST and amniotic fluid volume assessment Doppler velocimetry in IUGR
• 39. 39 The frequency of monitoring should be individualized depending upon the severity and presence of IUGR. Delivery Delivery is the only definitive treatment for pre-eclampsia and usually labour is induced at 38 weeks. Early termination may be needed if there is progression to severe eclampsia and eclampsia with worsening of either maternal or fetal condition. Antenatal corticosteroid to accelerate lung maturity in preterm. If there are no obstetric indication for caesarean section labour can be induced If the cervix is favorable with bishop’s score labour can be induced by ARM followed by oxytocin infusion. If cervix is not favourable PGE2 gel can be used to ripen cervix. Continuous CTZ monitoring is preferred during labour. Prophylactic Ergometrine is avoided as it leads to sudden rise in blood pressure Common anti hypertensive drugs Name Mode of action Dosage Side effects α methydopa Central action 1000-2000mg/day 3-4 divided doses Postural hypotension, CNS depression, Hemolytic anemia Nifedipine Ca channel blocker 20-40mg/day 2-4 divided doses Headache, flushing, palpitation Hydralazine Peripheral vasodilation 50-300mg.day 2-3 doses Headache, flushing, tachycardia, lupus Labetalol Combined α and β blocker 200-400mg/day 2 doses Postural hypotension, tremors Atenolol β blocker 50-200mg.day 1-2 doses Bradycardia, hypotension, hypoglycaemia, fatigue, IUGR *Note: Methyldopa is drug of choice ACE inhibitors absolutely contraindicated
• 40. 40 Severe Pre eclampsia Management In Severe Pre eclampsia, there is deterioration of either maternal or fetal condition or both and the definitive treatment is delivery after 34 weeks, severe pre eclampsia is best treated with termination especially if there is worsening of biochemical parameters. In cases before 34 weeks if the initial condition stabilizes there may be place for management. Severe Pre eclampsia before 24 weeks is best managed with termination of pregnancy. Antepartum Management The aim of expectant management is to protect mother and fetus from the consequences of the disease and at the same time prolong pregnancy if possible to avoid the dangers to the fetus of prematurity. The expectant management is abandoned if immediate termination uis decided 1. Anti hypertensive: Indicated to prevent cerebral hemorrhages, α methydopa and nifedipine are commonly used. Hydralazine and labetalol can also be used. 2. Close monitoring: Close monitoring of materal and fetal condition is performed Blood pressure and urine albumin daily Peripheral Blood Smear, platelet count, coagulation profile, uric acid, renal and liver functions tests on alternate days and in fulminant cases twice daily Fetal Daily fetal movement count Ultrasound to assess fetal growth and well-being NST and amniotic fluid volume assessment Doppler velocimetry in IUGR .poor oxygen saturation can occur in pulmonary edema and so continuous measurement of oxygen saturation using pulse oximetry is indicated in such cases 3. Antenal Corticosteroids: to accelerate lung maturity of fetus
• 41. 41 Criteria for Immediate Termination of pregnancy No reassuring fetal heart status Ruptured membrane Uncontrollable BP Oligohydramnios, with amniotic fluid index (AFI) of less than 5 cm Severe intrauterine growth restriction in which the estimated fetal weight is less than 5% Oliguria (< 500 mL/24 hr) Serum creatinine level of at least 1.5 mg/dL Pulmonary edema Shortness of breath or chest pain with pulse oximetry of < 94% on room air Headache that is persistent and severe Right upper quadrant tenderness Development of HELLP syndrome Intrapartum Management 1. Control of blood pressure : The diastolic pressure should not cross 100 mm Hg. Labetalol can be used as IV infusion 2mg over 2 min or bolus over 2 min. Hydralizine 5 mg bolus Iv injestion can also be given for acute control of blood pressure. Sublingual nifedine can be given but side effect is sudden drop of blood pressure. Rapid fall of blood pressure should be avoided as it may affect fetus. If diastolic blood pressure is 110mmHg, antihypertensive drugs are given Goal of antihypertensive therapy is to manage blood pressure up to 90-100 mmHg to prevent cerebral hemorrhage. Drug of choice Hydralazine 5 mg slowly over 5 min Nifedipine 12.5mg IM every two hourly as needed Labetelol and Nifedipine 10 mg IV after 10 mins (diastolic blood pressure increase 110mmHg) Labetelol 20 mg IV given Dose can be increased up to 40 mg and then 80 mg if not maintained after 10 minutes Nifedipine 5mg sublingually after 10 minutes 5 mg sublingually if BP not lowered
• 42. 42 2. Anticonvulsants: Prophylactic Magnesium sulphate can be given to prevent eclampsia in severe Pre eclampsia as MAGPIE trial. Dose of MgSO4 - Loading dose 4gm 20% MgSO4 IV over 5 minutes - follow 10gm 50% MgSO4, 5gm in each buttock as deep IM injection with 1 ml of 2% lignocaine in same syringe Apply aseptic technique while administering MgSO4 deep IM Patient may feel warm and flushing after administration of MgSO4 If convulsant reoccur 2gm of 50% MgSO4 IV over 5 minutes Maintenance Dose - 5gm of 50% MgSO4 in 1ml 2% lignocaine by same syringe four hourly in alternate buttocks - Continue treatment with MgSO4 for 24 hours after delivery or last convulsion Adverse Effects of MgSO4 Flushing Sweating Hypotension Depressed reflexes Flaccid paralysis Hypothermia Circulatory collapse CNS depression hypocalcaemia with tetany Contraindication Decreased blood pressure
• 43. 43 Respiratory arrest Disappearance of patellar reflex Precaution Respiratory rate < 16/ min Platellar Reflex present Urinary output at least 30ml/hr over 4 hours (if urinary output decreases MgSO4 absorption increases in blood and results increased toxic effects) Antidote (if toxic effect presents) - Assist ventilation (emergency drugs and intubation) - 10 ml 10%, 1 gm calcium gluconate IV slowly until respiratory rate returns to normal Diazepam If MgSO4 absent, diazepam can be used Diazepam is not a safe drug as it causes neonatal respiratory depression as it passed through placenta Long term IV use may cause respiratory depression in babies suffering from ischaemia due to placental compression and preterm birth. Loading dose 10mg IV slowly over 2 min convulsion reoccurs Repeat dose again Maintenance dose 40mg in 500ml IV in NS/RL If dose exceeds 30 mg / hr maternal respiratory depression occurs Dose should not exceed 100mg in 24 hours Ventilation should be assessed and assisted while administering diazepam. Rectal dose when IV not accessible Loading dose: 20mg in 10 ml syringe. if convulsions not controlled within 10 minutes 10mg/hr or more
• 44. 44 3. Fluid management Despite the presence of peripheral edema, patients with preeclampsia are intravascularly volume depleted, with high peripheral vascular resistance. Diuretics should be avoided. Aggressive volume resuscitation may lead to pulmonary edema, which is a common cause of maternal morbidity and mortality. Pulmonary edema occurs most frequently 48-72 hours postpartum, probably due to mobilization of extravascular fluid. Central venous or pulmonary artery pressure monitoring may be indicated in critical cases. A central venous pressure (CVP) of 5 mm Hg in women with no heart disease indicates sufficient intravascular volume, and maintenance fluids alone are sufficient. Total fluids should generally be limited to 80 mL/h or 1 mL/kg/h. Careful measurement of fluid input and output is advisable, particularly in the immediate postpartum period. Many patients will have a brief (up to 6 h) period of oliguria following delivery; this should be anticipated and not overcorrected. 4. Corticosteroids: Corticosteroids are indicated in HELLP syndrome. The other indication is to accelerate lung maturity of fetus. Obstetric Management Delivery is the only specific management of severe eclampsia and eclampsia Delivery should be conducted regardless of week of gestation if maternal or fetal condition worsens. Woman’s condition re establishes to normal within few hours after delivery and after 24 hours most of the symptoms regress. In severe eclampsia delivery should be conducted within 24 hours and in eclampsia within 12 hours. Assess cervix, if unfavorable induce (prostaglandin, misoprostol to ripen cervix) If favorable membrane rupture, augmentation Caesarean Section If FHR abnormal (less than 100 or more than 180b/min), Caesarean section is done
• 45. 45 Cervix is unfavorable and fetal is alive, Caesarean section is done, IUFD, too premature for survival, dead baby or absence of safe anesthetic drugs vaginal delivery is planned Indication of Caesarean Section Associated obstetric indications Failure induction Rapid worsening of maternal condition and delivery not imminent Fetal distress or severe IUGR Postpartum Management Prophylactic ergometrine and methargin are contraindicated and instead oxytocin or PGF2α can be used. These patients have contracted blood volume and there are more chances of PPH and shock so fluid management should be done. Cross matched blood should be kept ready. Oliguria is common after delivery but usually subsides, aggressive fluid replacement is avoided. the post partum period is crucial and continuous monitoring of biochemical and hematological parameters are required. This is because HELLP syndrome can occur in Postpartum period as well. Magnesium Sulphate is continued for another 24 hours. Antihypertensive drugs are continued in postpartum period as well. Methyldopa is avoided in post partum as it may cause depression Nifedipine and beta blockers like atenolol are prescribed. Medicines are stopped after 6 weeks. If hypertension persists cause is ruled out and woman is counseled for re occurrence of PIH and pre-eclampsia in next pregnancy and prophylaxis with low dose aspirin is considered in next pregnancy.
• 46. 46 Management done in my patient My patient was admitted with diagnosis of PIH but later she developed severe eclampsia followed by HELLP syndrome. Antenal Management Initially she was managed with methyldopa but when blood pressure was not controlled and patient’s condition progressively deteriorate MgSO4 and depin were added to course of treatment for blood pressure regulation and prevent impending eclampsia along with fluid management. Intranatal Mangement Though my patient had 26 WOG she wanted to continue pregnancy but later her condition worsened and she developed HELLP syndrome thus, medical termination of pregnancy was done at 26+5 WOG by inducing labour with misoprostol and oxytocin. Postnatal Management Daily hematological and biochemical parameters were monitored to evaluate HELLP syndrome, patient had Oliguria thus, fluid management was continued in postpartum along with anti hypertensives and MgSO4. Two pint blood was transfused to treat anemia as her Hb level dropped to 7 mg/dl Injection Rhogam was administered for prophylaxis All symptoms subsided 5 days after MTP and patient was discharged HELLP Syndrome It is acronym for hemolysis (H), Elevated Liver Enzymes (EL) and Low Platelet count (LP) (<100,000/mm³) this is a rare complication of pre eclampsia (10-15%). HELLP syndrome may develop even without maternal hypertension. This syndrome is manifested by nausea, vomiting, Epigastric pain or right upper quadrant pain along with biochemical and hematological changes. Parenchymal necrosis of liver causes elevation of hepatic enzymes (AST and ALT >70 IU/L, LDH>600 IU/L) and Bilirubin (>12 mg/dl). There may be subcapsular haematoma formation (which is diagnosed by CT scanning) and abnormal peripheral blood smear. Eventually liver may rupture to cause sudden hypotnsion, due to hemoperitoneum.
• 47. 47 Management Principle of management same as severe pre eclampsia and eclampsia. Anti seizure prophylaxis with magnesium sulphate is started. Assessment of maternal and fetal condition followed by delivery is done. Corticosteroids are administered as it improves perinatal ( increase pulmonary maturity, decrease IVF and necrotizing enterocolitis) and maternal (increase thrombocyte count and increase urinary output) outcome. Caesarean section is the most common mode of delivery. Epidural anesthesia can be used if platelet count is >1,00,000/ mm³. Platelet transfusion is done if the count is <50,000/mm³. patient should be managed at ICU until there is improvement in platelet count, urine output, BP and liver enzymes. recurrent risk of HELLP syndrome is 3-19% Expectant Management: it has been carried out selectively when pregnancy is <34 weeks, with bed rest, plasma volume expansion (infusion of 5-25% albumin),, antithrombotic agents (dipyridamole), immunosuppressive agents (steroids) and others ( fresh frozen plasma). In HELLP syndrome perinatal mortality ranges between 5-60% and maternal mortality up to 25% Complications Maternal: abruption placenta, DIC, acute renal failure, severe ascites, pulmonary edema,pleural effusions, cerebral edema, laryngeal edema, retinal detachment, subcapsular hematoma, ARDs, sepsis and death Perinatal: morbidity and mortality are significantly increased this is due to pre term delivery, prematurity, RDS and sepsis
• 48. 48 PROGNOSIS Pre-eclampsia is usually insidious in onset and runs a slow course. Rarely onset may be acute and follows a rapid course of events. The prognosis of pre-eclampsia depends on the period of gestation, severity of disease and response to treatment The following courses may occur: If detected early: with prompt and effective treatment the pre-eclamptic features may subside completely If left untreated: a. The Pre-eclamptic features remain stationary at varying degrees till delivery b. Aggravation of the pre-eclamptic features with appearance of symptoms of acute fulminating pre-eclampsia. Most commonly occurs in cases with acute onset c. Eclampsia d. Spontaneous remission of Pre-eclamptic features
• 50. 50 NURSING MANAGEMENT Assessment a. History Taking: including patient’s chief complain, present health status, birth history, family history, onset of sign and symptoms (increased blood pressure, edema, headache, epigastric pain, nausea and vomiting, blurred vision). Previous History of Preganacy: Previous history of pregnancy with preeclampsia or eclampsia before. b. Physical Examination: Skin pale and yellowish, Bilateral pedal edema present, Peri- orbital edema present around eyes, no hepatomegaly and spleenomegaly, increased blood pressure monitor fetal heart rate to determine fetal distress, assess patellar reflex c. Investigations: vital signs: blood pressure every two hourly in both arm laboratory: urine protein increased to +3, decreased Hematocrit , increased serum creatinine, BUN, SGOT, SGPT, platelets Level of consciousness: reduced GCS Ultrasound: to evaluate fetus condition Nursing diagnosis Ineffective Cerebral Tissue Perfusion related to decreased cardiac output secondary to vascular vasopasm. Impaired Gas Exchange related to accumulation of fluid in the lungs pulmonary edema. Activity Intolerance related to weakness. Self care deficit related to decreased strength and endurance as evidenced by inability to ambulate independently Impaired Urinary Elimination related to impaired glomerular filtration as evidenced by anuria and oliguria Risk for Injury related to diplopia and increased intra-cranial pressure, seizures.
• 51. 51 Risk for impaired skin integrity related to impaired physical mobility and invasive procedure (deep IM injections) Knowledge Deficit related to the management and treatment of disease Planning/ Goal The major goals are to maintain adequate cerebral tissue perfusion by lowering blood pressure, maintain effective gas exchange, increase activity tolerance, encourage and assist patient on Activities Of Daily Livings (ADLS), maintain fluid status, prevent patient from potential injuries caused by seizure activities, maintain skin integrity and provide education regarding management of disease Interventions 1. Ineffective cerebral tissue perfusion Monitor neurological status and compare it to normal state. Monitor vital signs. Record changes such as the blindness of vision, or visual field disturbances in perception. Assess the higher functions, such as speech function. Put head slightly elevated position. Maintain a state of bed rest, Create peaceful environment; limit the activities of visitors or patients as indicated. Provide oxygen therapy as indicated 2. Impaired gas exchange Encourage deep breathing and coughing exercise Elevate head of bed to semi-fowler’s position Avoid restrains Administer oxygen therapy as indicated Stop MgSO4 immediately if sings of respiratory occurs
• 52. 52 3. Activity Intolerance Assess patient's level of mobility Assess potential for physical injury with activity (falls or overexertion) Assess patient's cardiopulmonary status before activity Assist for ambulation and short range of motion exercises as tolerant by patient 4. Self care deficit Assess client level to perform ADLS Assist client with daily activities Provide positive reinforcement during activity. Allow patient to perform tasks at his or her own rate Encourage independent activity as able and safe 5. Impaired Urinary output Assess the signs of fluid volume excess, respiratory distress due to pulmonary edema Monitor input output strictly Avoid over resuscitation of fluid Change patients position frequently Administer IV fluids as prescribed 6. Risk for Injury Monitor blood pressure every 2 hourly Record the patient's level of consciousness Assess signs of eclampsia (hyper active, the patellar reflexes, decreased pulse and respiration, epigastric pain and oliguria) Monitor for signs and symptoms of labor or uterine contractions. Administer antihypertensive as prescribed to reduced blood pressure
• 53. 53 7. Risk for impaired skin integrity Maintain adequate fluid intake Elevate lower extremities to decrease edema Keep bed sheets clean and dry, tug bed sheets properly and avoid wrinkles Inspect skin surfaces to assess skin breakdowns Change position every two hourly Provide back care 8. Knowledge Deficit Give education regarding home based management of disease Provide health education regarding diet modifications Provide information’s regarding drug dosage and it’s adverse effects
• 54. 54 APPLICATION OF NURSING THEORY While providing care to my patient, I applied Orem’s Theory of Nursing. Orem’s Theory consists of 1. Theory of self care 2. Theory of self care deficit 3. Theory of Nursing System My patient Bimala Gurung, 29years female was admitted on Gynaecology ward of Kist Medical Teaching Hospital with diagnosis of Pregnancy induced Hypertension with Severe Pre-eclampsia with HELLP syndrome. Before termination of pregnancy my patient’s condition was critical, and was partly conscious, she was pale, weak and was in need of assistance to meet her needs but after pregnancy her condition gradually progressed and she was able to carry out activities of daily living by herself and needed no assistance to meet her needs. Thus, I applied Orem’s theory as it appeared to be the best possible theory to meet my client’s need while providing nursing care. Orem’s Theory of Nursing Care Orem’s theory of nursing has three related theories 1. Theory of self care 2. Theory of self care deficit and 3. Theory of nursing system By assessing condition of my patient I figured out theory of nursing system as most suitable theory for caring my patient Theory of nursing system. It describes how the patients self care needs will be met by the nurse, patient and both It identifies three classifications of nursing system to meet the self care requisites of the patient - Wholly compensatory system - Partly compensatory system - Supportive- educative system
• 55. 55 Wholly compensatory nursing system is represented by a situation in which the individual is unable to engage in self care actions requiring self directed and controlled ambulation and manipulative movement or the medical prescription to refrain from such activities Person with these limitations are socially dependent on others for their continued existence and wellbeing. Example patient in coma Partly compensatory nursing system represented by a situation in which both nurse and patient perform care measures or other action involving manipulative tasks or ambulation. Either patient or nurse may have major role in performance of self care measures. Examples a person who recently had surgery Supportive- educative system: in this system the person is able to perform or can and should learn to form required measures of externally or internally oriented therapeutic self care but cannot do so without assistance. This is also known a supportive developmental system. In this system patient is doing all of his self care. The patient’s requirements for help are confined to decision makings behavior control, and acquiring knowledge and skills. The nurse’s role is to promote the patient as a self care agent. Example chronic disease patients like hypertension I applied Partly compensatory by - By providing all self care activities like mouth care, back care when my patient was partly conscious - Her elimination need was fulfilled by catheterization - Medication - Providing safe environment And I applied supportive educative theory by - Providing information about disease condition - Medication - Complication and it’s prognosis - Home based management of disease and possible risks - Diet - Follow up
• 56. 56 NURSING CARE PLAN Demographic Data Name of patient: Bimala Gurung Age: 29 years Sex: Female Caste: Gurung Religion: Hindu Marital status: Married No. of Children: 1 Date Of Admission: 2070/1/19 Inpatient number: 19381 Medical Diagnosis: Provisional Diagnosis: G3P2L1 at 26+4 WOG with PIH Final Diagnosis: Pre-eclamsia with HELLP syndrome Assessment My patient presented with chief complain of amenorrhea for last six months, Epigastric pain for 1-2 hours, vomiting two episodes and headache on emergency and was admitted with diagnosis of PIH but later she developed severe eclampsia followed by HELLP syndrome. My patient had fetus with 26 WOG she wanted to continue pregnancy but later her condition worsened and she developed HELLP syndrome thus, medical termination of pregnancy was done at 26+5 WOG by inducing labour on 2070/1/21 All symptoms subsided 5 days after MTP and patient was discharged Nursing Diagnosis Ineffective Cerebral Tissue Perfusion related to decreased cardiac output secondary to vascular vasopasm. Impaired Gas Exchange related to accumulation of fluid in the lungs pulmonary edema. Activity Intolerance related to weakness. Self care deficit related to decreased strength and endurance as evidenced by inability to ambulate independently Impaired Urinary Elimination related to impaired glomerular filtration as evidenced by anuria and oliguria Risk for Injury related to diplopia and increased intra-cranial pressure, seizures. Risk for impaired skin integrity related to impaired physical mobility and invasive procedure (deep IM injections) Knowledge Deficit related to the management and treatment of disease
• 57. 57 S.N. Assesment Nursing Diagnosis Nursing Goal Nursing intervention Rationale Evaluation 1 Subjective data: I feel dizziness Objective data: - Partly conscious - No response to verbal command - Impaired communication - Not oriented to time place and person Ineffective Cerebral Tissue Perfusion related to decreased cardiac output secondary to vascular vasopasm. Maintain effective cerebral tissue perfusion with no signs of impaired GCS within 4 hours of intervention Monitor neurological status and compare it to normal state. Monitor vital signs. Record changes such as the blindness of vision, or visual field disturbances in perception. Assess the higher functions, such as speech function. Put head slightly elevated position. Maintain a state of bed rest To detect early signs of impaired cerebral tissue perfusion Assess condition of patient. Indicates neurological impairment and impaired tissue perfusion To assess neurological status and plan early intervention To improve blood circulation and decrease blood flow resistance To prevent potential Goal met patient’s condition was stabilized after intervention as evidenced by increase verbal communication and regain of consicousness
• 58. 58 Create peaceful environment Limit the activities of visitors or patients as indicated. Provide oxygen therapy as indicated injuries To provide rest to patient To eliminate fatigue and agitation To improve tissue perfusion 2 Subjective Data: I have chest pain while breathing Objective Data: Respiratory Rate: 32/m SpO2 86% without oxygen sign of cyanosis: bluish lips seen Impaired Gas Exchange related to accumulation of fluid in the lungs pulmonary edema. Maintain gas exchange and oxygen saturation with in 3 hour Encourage deep breathing and coughing exercise Elevate head of bed to semi- fowler’s position Avoid restrains Administer oxygen therapy as indicated Stop MgSO4 immediately if sings of respiratory occurs Promotes chest expansion Facilitates respiratory function by use of gravity It may cause agitation with increased cardiac workload MgSO4 toxicity causes depression of respiratory centre To maintain oxygen Goal met oxygen saturation was maintained at 96% with oxygen at 2l/min
• 59. 59 Administer oxygen at 2l/min saturation 3 Subjective data: I can’t do it, I feel weak Objective data: Decreased activity Weak appearance Activity Intolerance related to weakness. Increase tolerance to simple activity after 2 hour Assess patient's level of mobility Assess potential for physical injury with activity (falls or overexertion) Assess patient's cardiopulmonary status before activity Assist for ambulation and short range of motion exercises as tolerated To assess patient’s condition To prevent potential hazards To assess patients ability to carry out activities To gradually increase tolerance to activities and make patient independent Goal met as patient did short range of motion exercises and tolerated the exertion after encouraging her 4 Subjective data I have difficulty doing works Self care deficit related to decreased strength and endurance as evidenced by inability to ambulate independently Provide and assist in self care activities Assess client level to perform ADLS Assist client with daily activities Provide positive To obtain baseline data and evaluate patient’s ability To maintain hygiene and promote comfort To encourage client Goal met , patient’s hygiene was maintained after assisting her and encouraging her it perform it by herself
• 60. 60 Objective data: Patient cannot mobilize and carry out activities by herself reinforcement during activity. Allow patient to perform tasks at his or her own rate Encourage independent activity as able and safe and build up positive attitude To maintain client’s self esteem To promote client’s ability 5 Subjective data: - Objective data: urine output less than 30ml/hour Generalized edema Impaired Urinary Elimination related to impaired glomerular filtration as evidenced by anuria and oliguria Maintain fluid volume and increase urine output to 30ml/hour within 24 hour Assess the signs of fluid volume excess, respiratory distress due to pulmonary edema Monitor input output strictly Avoid over resuscitation of fluid Change patients position frequently Administer IV fluids Intravascular fluid is contracted and sudden shift of fluid into intravascular compartment causes fluid volume excess To monitor Oliguria and maintain fluid balance To avoid complication like pulmonary edema To maintain fluid volume with gravity To manage persistent Oliguria Gal was met as Oliguria subsided 24 hour after MTP
• 61. 61 6 Subjective data: - Objective data: Diplopia and blurring of vision due to pressure caused on small capillaries of eye Increased blood pressure Risk for Injury related to diplopia and increased intra-cranial pressure, seizures. Patients remains free of injury Monitor blood pressure every 2 hourly Record the patient's level of consciousness Assess signs of eclampsia (hyper active, the patellar reflexes, decreased pulse and respiration, epigastric pain and oliguria) Monitor for signs and symptoms of labor or uterine contractions. The pressure over 110 mmHg diastole and systole 160 or more an indication of PIH. The decline of consciousness as an indication of decreased cerebral blood flow. The symptoms are a manifestation of changes in the brain, kidney, heart and lung that precedes seizure status. Seizures will increase the sensitivity of the uterus which will allow the delivery. Goal met as patient didn’t had any seizure episodes and remained free from injuries
• 62. 62 Administer antihypertensive as prescribed to reduced blood pressure Anti-hypertension to lower blood pressure. 7 Subjective data: - Objective data: prolonged immobilization redness on back sacral area Ecchymosis on buttocks due to IM injection given Risk for impaired skin integrity related to impaired physical mobility and invasive procedure (deep IM injections) Maintain skin integrity Maintain adequate fluid intake Elevate lower extremities Keep bed sheets clean and dry, tug bed sheets properly and avoid wrinkles Inspect skin surfaces to assess skin breakdowns Change position every two hourly Provide back care To maintain turgor of skin To decrease fluid volume in Extracellular compartment and decrease edema To reduce shearing force of linen and prevent skin breakdown To detect early signs of skin breakdown To prevent bed sore and maintain skin integrity Goal met patient showed no signs of skin breakdown and pressure sores
• 63. 63 8 Subjective data: We don’t know what precaution we should take after being discharged Objective data: - Knowledge Deficit related to the management and treatment of disease Provide knowledge regarding home based management of disease Give education regarding home based management of disease Provide health education regarding diet modifications Provide informations regarding drug dosage and it’s adverse effects To manage disease at home To prevent complications and lead a healthy life style To maintain drug compliance and manage side effects of drugs Goal met, patients and visitors were given teching regarding home based management of PIH and pre eclampsia
• 64. 64 Diversional Therapy Diversional therapy is a kind of therapy which is used to distract the mind of the patient. hospital environment causes stress and anxiety to both patient and family. Hospital is new environment for both patient and family. Hospital stay might be more frustrating to patient as she has to undergo through various investigations and medicine on daily basis it may make patient more anxious thus, to divert mind from such anxiety diversional therapy is used to reduce stress and maintain mental health of patient and it is very useful for the full recovery of patient. My patient was anxious about the disease condition especially regarding condition of fetus thus I applied talk therapy, distraction therapy and deep breathing therapy. Talk Therapy: It is the best way to verbalize patient feeling, sharing and communicating one’s feeling and anxiety. I used talk therapy to divert her mind and express her anxiety regarding disease prognosis it’s re occurrence and fetal condition. She shared her feelings and I reassured that she might be able to recover fully and disease have very good prognosis after delivery Distraction therapy To distract patient’s mind I asked visitors to talk with her and provide her support, talk about her interest and her daughter. Deep breathing and relaxation therapy This is the most simple and beneficial relaxation therapy, in this therapy client is asked to take deep breaths and relax all abdominal and respiratory muscles, it improves respiratory function of body as well as distracts client.
• 66. 66 DRUGS USED IN MY PATIENT SN Drugs Dose Route Frequency 1. Tab Iron 500mg PO OD 2. Tab Calcium 400mg PO OD 3. Tab Methyldopa 500mg PO TDS 4. Inj Magnesium Sulphate 4gm (20%) followed by 5gm (50%) IV Deep IM on alternate buttocks Stat 4 hourly over 24 hours 5. Tab Aciloc 150mg PO BD 6. Tab Pentodac 40mg PO OD 7. Tab Depin 50mg PO OD 8. Tab Miso 100mg 50mg PV Stat 4 hourly 9. Inj Syntocin 5U in RL IV Starting from 10 drops/min upto 40 drops 10. Tab Amlodipine 5mg PO OD 11. Syrup Lactulose 10ml PO TDS 12. Inj. Durataz 4.5gm IV BD 13. Tab B-long 2Tab PO TDS 14. Inj Rhogam 1 amp IV Stat 15. Tab Cefexime 400 mg PO BD
• 67. 67 Iron Trade name: E-fol Generic name: Ferrous Suphate Group: Minerals Iron is a micronutrient, it is essential for formation of haemoglobin. Mechanism of action It is essential micronutrient for formation of haemoglobin. It’s product haem combines with globulin to produce hemoglobin Indication Anemia, pregnancy and puerperim Preparation tablet and iron dextran Usual Dose 100-200 mg of iron in divided doses can be given parenterally where oral therapy cannot be taken as iron dextran Treatment should be continued until haemoglobin reach normal citric acid and ascorbic acid increase its absorption Contraindication During 1st trimester of pregnancy, patient under tetracycline and antacids Side effect GIT: abdominal discomfort, constipation, black stool Nursing consideration Ascorbic acid increases absorption of iron. Consuming citrus fruit or tomato juice with iron preparation may increase its absorption.
• 68. 68 Milk, eggs, or caffeine beverages inhibit absorption. Increase fluid intake Iron preparations cause dark green or black stools. Report constipation or diarrhea Encourage fiber and roughage containing diet Calcium Trade name: Calvit Generic name: Calcium phosphate Group: Minerals Mechanism of action It helps in contraction of muscles and transmission of nerve impulses from nerve endings to muscle fibers and in clotting of blood. It is important component of teeth and bones. Vitamin D and some hormones controls absorption and excretion of calcium from kidney, parathyroid hormone and calcitonin control the regulation of calcium Indication Hypocalcaemia in tetany, rickets, hyperkalemia, osteomalacia, pregnancy, cardiac arrest, chronic renal disease Preparation Calcium Sachet Calcium Tablet Calcium Chewable Tablet Usual Dose Adult: 800mg/Day Pregnancy Lactation: 1200 Mg/Day
• 69. 69 Contraindication Renal Stone Side Effect Respiratory: Bronchospasm Skin: Rash, Itching GIT: Constipation CVS: Bradycardia, Cardiac Arrhythmias Nursing Consideration Increase fluid intake Methyldopa Trade name: Dopamet Generic name: α-methyl-L-dopa Group: Centrally acting anti hypertensives Mechanism of action Although the mechanism of action has yet to be conclusive , the resultant hypotensive effect is due to the drug's action on the CNS. Methyldopa is converted into the metabolite, alpha- methylnorepinephrine, in the CNS, where it stimulates the central inhibitory alpha-adrenergic receptors, leading to a reduction in sympathetic tone, total peripheral resistance, and blood pressure. Reduction in plasma renin activity, as well as the inhibition of both central and peripheral norepinephrine and serotonine production may also contribute to the drug's antihypertensive effect, although this is not a major mechanism of action. This is done through the inhibition of the decarboxylation of dihydroxyphenylalanine (dopa)—the precursor of norepinephrine—and of 5-hydroxytryptophan (5-HTP)—the precursor of serotonin—in the CNS and in most peripheral tissues.
• 70. 70 Indication For use in the treatment of hypertension. Preparation Tablet 125mg, 250mg, 500mg Usual Dose Initially: 250mg orally 2 to 3 times a day increased gradually at intervals of at least 2 days (maximum 3gm/day) initially 125mg twice daily in the elderly Contraindication Active Liver Disease, Phaecochromocytoma Depression Side effect Sedation, Depression, Nightmare, Headache, Fever, Dry Mouth, GI Upset, Hemolytic Anemia, Hepatitis, Nasal Stiffness, Edema, Parkinsonism, Gynaecomastia, Lactation,Rashes, Blood Dycariasis, Positive Coomb’s Test Nursing consideration - If sign of orthostatic hypotension and other adeverse effect develop, give medicine at - bedtime - Warn patient to avoid hazardous activities that require mental alertness until sedative effect subside - Weight patient daily, salt and water retention may occur but can be relieved by diuretics
• 71. 71 Magnesium sulphate Trade name: Magnesuim Sulphate Generic name: Magnesuim Sulphate Group: Anti convulsant Mechanism of action It increases cerebral blood flow as established by Doppler studies. It reduces cerebral vasospastic ischemia. Elevated concentration of circulatory magnesium decreases the acetylcholine release and reduces the motor plate sensitivity to acetylcholine. This therapy reduces neuromuscular irritability It also decreases intracranial edema and helps in dieresis. Its peripheral vasodilation effect improves the uterine blood supply Indication Severe Pre eclampsia Eclampsia Preparation Injection (50%) 2mmol Mg++/ml ampoule 10ml (5gm) Usual Dose - Loading dose 4gm 20% MgSO4 IV over 5 minutes - follow 10gm 50% MgSO4, 5gm in each buttock as deep IM injection with 1 ml of 2% lignocaine in same syringe Apply aseptic technique while administering MgSO4 deep IM Patient may feel warm and flushing after administration of MgSO4 If convulsant reoccur 2gm of 50% MgSO4 IV over 5 minutes Maintenance Dose - 5gm of 50% MgSO4 in 1ml 2% lignocaine by same syringe four hourly in alternate buttocks - Continue treatment with MgSO4 for 24 hours after delivery or last convulsion
• 72. 72 Adverse Effects of MgSO4 Flushing, Sweating, Hypotension, Depressed reflexes, Flaccid paralysis, Hypothermia, Circulatory collapse, CNS depression, hypocalcaemia with tetany Contraindication Decreased blood pressure Respiratory arrest Disappearance of patellar reflex Precaution Respiratory rate < 16/ min Platellar Reflex present Urinary output at least 30ml/hr over 4 hours (if urinary output decreases MgSO4 absorption increases in blood and results increased toxic effects) Nursing consideration - Monitor and assess respiratory status, depth and rate - Assess patellar reflex (knee jerk) as high dose leads to muscular paresis in this case medicine should be withheld - Assess vital sign strictly - Maintain input output chart, urine output should be more than 30ml/hr - Renal function must be monitored - Inj calcium gluconate should be at hand in case of high dose
• 73. 73 Aciloc Trade name: Aciloc Generic name: Ranitidine Group: H2 receptor antagonist Mechanism of action It inhibits action of histamine at H2 receptor by blocking the receptor. This prevents histamine from combining to H2 receptors. Thus, histamine will be unable to stimulate the secretion of proton (H+) which combines with chloride in stomach and produce HCL. This leads to reduction of acidity and increase pH. Indication Used in the treatment of peptic ulcer disease (PUD), dyspepsia, stress ulcer prophylaxis, and gastroesophageal reflux disease (GERD). Preparation Ranitidine Tablet 150mg, 300mg Ranitidine Injection 25mg/dl Usual Dose 150 Mg BD For 4-6 Weeks Beningn Gastric Ulcer Or Duodenal Ulcer 300mg Orally At Night For 4-8 Weeks Maintenance 150mg Orally At Night IV 50mg 6-8 Hourly Contraindication hypersensitivity, lactation, preganancy, renal/hepatic disease Side effects CNS: headache, dizziness, confusion, malaise, drowsiness CVS: bradycardia or tachycardia, hypertension
• 74. 74 GIT: nausea, vomiting, diarrhea, hepatitis, abdominal pain Genitourinary: impotence Eye: ocular pain, blurred vision Nursing consideration - Administer Iv slowly, if possible dilute with distilled water over 5 minutes - Dosage adjustment for patients with impaired Renal function - Instruct patient to take drugs as directed, even after pain subsides to ensure proper healing -If patient is taking single dose advice to take at bed time Pentodac Trade name: Pentodac, Pantop Generic name: Pantoprazole Group: Proton Pump Inhibitor Mechanism of action Pantoprazole is a proton pump inhibitor (PPI) that suppresses the final step in gastric acid production by forming a covalent bond to two sites of the (H+ ,K+ )- ATPase enzyme system at the secretory surface of the gastric parietal cell. This effect is dose- related and leads to inhibition of both basal and stimulated gastric acid secretion irrespective of the stimulus. Indication Used in the treatment of peptic ulcer disease (PUD), dyspepsia, stress ulcer prophylaxis, and gastroesophageal reflux disease (GERD). Preparation Tablet delayed releasing 20 mg, 40mg Powdered Injection 40 mg/vial Usual Dose 40mg/day for 8 weeks for erosive esophagitis if not healed continued for another 8 weeks
• 75. 75 Contraindication None Side effects Rare diarrhea, headache, dizziness, pruritus, skin rash Nursing consideration - Give tablet without regards to meal, tablet should not be chewed - Refrigerate vial, protect from sun - For reconstitution mix 40mg vial with 10ml 0.9% NaCl then further dilute with 100 ml 5% dextrose or NS or RL to have concentration of 0.4mg/ml - Do not refrigerate reconstituted once diluted, solution I stable for 12 hours Depin Trade name: Depin Generic name: Nifedipine Group: Calcium Channel Blockers Mechanism of action Nifedipine decreases arterial smooth muscle contractility and subsequent vasoconstriction by inhibiting the influx of calcium ions through L-type calcium channels. Inhibition of the initial influx of calcium inhibits the contractile processes of smooth muscle cells, causing dilation of the coronary and systemic arteries, increased oxygen delivery to the myocardial tissue, decreased total peripheral resistance, decreased systemic blood pressure, and decreased afterload. The vasodilatory effects of nifedipine result in an overall decrease in blood pressure. Indication For the management of vasospastic angina, chronic stable angina, hypertension, and Raynaud's phenomenon. May be used as a first line agent for left ventricular hypertrophy and isolated systolic hypertension (long-acting agents).
• 76. 76 Preparation Capsules (5mg, 10mg) tablet depin retard (10mg, 20mg) Usual Dose 5-20mg 3 times a day with or after meals, 10-20mg BD as sustained release (SR) with or after meals Contraindication Cardiogenic Shock, Acute MI, Hypertension in Pregnancy Side effect Headache, dizziness, flushing, palpitation, edema, lethargy, gum hyperplasia Precaution Inheart failure, severe hypotension, diabetes mellitus, liver disease, lactation Nursing consideration - 4 hourly BP should be taken and recorded - Drugs should be reduced slowly - Tablet should not be chewed - Tell patient about hypotensive effects during adjustments Misoprostol Trade name: Misoprostol Generic name: Misoprostol Group: Prostaglandin Mechanism of action It binds with prostaglandin receptors of uterus and help in uterine contration, frequency, ripening of cervix
• 77. 77 Indication Pregnant women with unfavourable cervices. This indication is avoided in women with prior uterine surgery or cesarean surgery due to an increased risk of possible uterine rupture. Misoprostol is also used for the prevention or treatment of serious postpartum hemorrhage. Preparation In form of tablet 100mcg and 200mcg Usual Dose 100-200mcg QID after meal at bed time labor induction 25mcg 3-6 hourly vaginally or bucally Contraindication pregnancy, lactation Side effect diarrhea, abdominal pain, appetite change, headache, anxiety, dysmennohea, miscarriage Nursing consideration - Give with food to minimize GI adverse effects - Store away from heat, light, and moisture. - Monitor for diarrhea; may be minimized by giving drug after meals and at bedtime. Diarrhea is a common adverse effect that is dose related and usually self-limiting
• 78. 78 Syntocin Trade name: Syntocin Generic name: Oxytocin Group: Anti-tocolytic Agents Oxytocin is an octapeptide secreted by posterior pituitary along with ADH. Oxytocin is a naturally occurring nanapeptide hormone. It has pronounced effects on uterine contraction and for this purpose it is used clinically to induce labour. Mechanism of action Binds the oxytocin receptor which leads to an increase in intracellular calcium levels. The oxytocin-oxytocin receptor system plays an important role as an inducer of uterine contractions during parturition and of milk ejection. It induces hypotension at high dose and decrease urine output Indication To assist in labor, elective labor induction, uterine contraction induction, reduction of postpartum haemorrhage and expulsion of placenta, incomplete abortion, increase mill secretion Preparation Injection oxytocin 5IU/ml (1IU of oxytocin = 2mcg of pure hormone) Usual Dose Induction and augmention of labour start 1-4 milliunit/min increasing the rate every 15-20 min to max of 20milliunit.min Postpartum haemorrhage Prevention IM5-10 units Treatment by slow IV injection 5 units, severe cases : by IV infusion 5-10 units in normal saline Contraindication hypersensitivity, pregnancy, severe toxaemia, obstructed labour, hypertonic uterus, placenta previa, fetal distress Side effect
• 79. 79 CNS: subarachnoid hemorrahage CVS: hypertension, tachycardia arrhthymias Blood: afibrinogenemia GIT: nausea, vomiting Miscellaneous: hypersensitivity, hypertonic uterine contraction, abruption placenta, impaired uterine blood flow, pelvic hematoma, increased uterine motility, uterine rupture and PPH Nursing consideration - Ensure continuous observation of patient receiving IV oxytocin for induction or stimulation of labor; fetal monitoring is preferred. A physician should be immediately available to deal with complications if they arise. - Regulate rate of oxytocin delivery to establish uterine contractions that are similar to normal labor; monitor rate and strength of contractions; discontinue drug and notify physician at any sign of uterine hyperactivity or spasm. - Ensure fetal position and size and absence of complications that are contraindicated with oxytocin before therapy. - Monitor maternal BP during oxytocin administration, discontinue drug and notify physician with any sign of hypertensive emergency. - Monitor neonate for the occurrence of jaundice. AMLODIPINE Trade name: Amlod Generic name: Amlodipine Group: Calcium channel blocker Mechanism of action Inhibits calcium movement across cell membrane of cardiac and vascular smooth muscles, dilates coronary arteries, decreases total vascular resistancy by vasodilation. Indication Hypertension
• 80. 80 Preparation Tablet: 2.5mg, 5mg, 10mg. Usual Dose For hypertension: initially 5mg/day as single dose, maximum 10mg/day. For angina: 5-10 mg:adult; 5mg:elderly Contraindication Severe hypotension, impaired hepatic function, aaortic stenosis, CFH. Side effect Peripheral edema, headache, flushing, dizziness, palpitation, nausea, asthenia. Nursing consideration Access BP, if systolic BO s below 90 mm Hg withhold medicine and inform to physician. Access the peripheral edema behind medical malleolus for fluid retention. Instruct patient as do not discontinue the medication abruptly. Avoid concomitant ingestion of grapefruit juice. Lactulose Trade name: Cephulac Generic name: lactulose Group: hyperosmotic laxative Mechanism of action Lactulose is a synthetic sugar used in the treatment of constipation and liver disease. It consists of the monosaccharides fructose and galactose. In the colon, lactulose is broken down primarily to lactic acid, and also to small amounts of formic and acetic acids, by the action of via evolved- beta galactosidase from colonic bacteria, which results in an increase in osmotic pressure and slight acidification of the colonic contents. This in turn causes an increase in stool water content and softens the stool. In treating heptic diseases (hepatic encephalopathy) lactulose draws out ammonia from the body in the same way that it draws out water into the colon.
• 81. 81 Indication Treatment of constipation Prevention and treatment of portal-systemic encephalopathy Preparation Syrup 10 g/15 ml Usual Dose Laxative: 15-30 ml/d PO; may be increased to 60 ml/d as needed. Portal-systemic encephalopathy 30-45 ml TDS or QID Contraindication known allergy to lactulose, low-galactose diet. Use cautiously with diabetes and lactation. Side effect GI: Transient flatulence, distension, intestinal cramps, belching, diarrhea, nausea Hematologic: Acid---base imbalances Nursing consideration - Give laxative syrup orally with fruit juice, water or milk to increase palatability. Do not freeze laxative form. Extremely dark or cloudy syrup may be unsafe; do not use - Administer retention enema using a rectal balloon catheter. Do not use cleansing enemas containing soap suds or other alkaline agents that counteract the effects of lactulose. - Do not administer other laxatives while using lactulose. - Monitor serum ammonia levels. - Monitor with long-term therapy for potential electrolyte and acid---base imbalances.
• 82. 82 Durataz It is active against betalactamase producing bacteria but not effective against pseudomonas, poteus and enterococci. It is highly protein bound (85%-90%). It is very commonly used drug in typhoid then switch over cefixime. It is administered parenterally only. Trade name: Xone, Taxim, Accutaz Durataz Generic name: Ceftriaxone Group: Cephalosporin Mechanism of action Inhibits bacterial growth by interfering with a specific step in bacterial call wall synthesis, probably by acylation of membrane bound transpeptidase enzyme. This prevents the cross linkage of peptidoglycon chains, which is necessary for bacterial wall synthesis. Indication salmonella typhi, gram negative infections resistant to usual antibiotics, endocarditis, chancroid, gonorrhea, meningitis Preparation Available in injections Ceftriaxone sodium injection 250mg, 500mg, 1gm Dose 1-2 g/d IV TDS or QID or in equal divided doses BD. Do not exceed 4 g/d. Adverse Effects Gastrointestinal: nausea/ vomiting, diarrhea, taste perversion, constipation Cardiovascular: vasodilatation Respiratory: Dyspnea Precaution use with caution in infants under 6 weeks of age
• 83. 83 Contraindication hypersensitivity Nursing Implication Use cautiously in patients with renal impairment, where dose adjustment is needed. Make sure patient does not have cephalosporin and penicillin allergy Patient are suggested to take a lot of water Advice patient to inform doctor immediately if allergy occurs B- long Trade name: B- long Generic name: Pyridonxine Group: Vitamin Mechanism of action Pyridoxine is the 4-methanol form of vitamin B6 and is converted to pyridoxal 5-phosphate in the body. Pyridoxal 5-phosphate is a coenzyme for synthesis of amino acids, neurotransmitters (serotonin, norepinephrine), sphingolipids, aminolevulinic acid. Indication For the treatment of vitamin B6 deficiency and for the prophylaxis of isoniazid-induced peripheral neuropathy. Preparation capsules, syrups and injection Usual Dose Pyridoxine deficiency: 10 to 25 mg/day orally, IM, or IV for 3 weeks followed by 2 to 5 mg/day from a multivitamin product. anemia: 200 to 600 mg orally daily
• 84. 84 Contraindication Hypersensitivity Rhogam Trade name: Generic name: Group: Immunoglobulin Mechanism of action Sterile nonpyrogenic gamma globulin solution containing immunoglobulins (IgG) of at least 90% IgG, which provides passive immunity by suppressing active antibody response and formation of anti- Rh (D) (isoimmunization) in Rh-negative individuals previously exposed to Rh-positive Effective for exposure in Rh-negative women when Rh-positive fetal RBCs enter maternal circulation during third stage of labor, fetal-maternal hemorrhage (as early as second trimester), amniocentesis, or other trauma during pregnancy, termination of pregnancy, and following transfusion with Rh-positive RBC, whole blood, or components (platelets, WBC) prepared from Rh-positive blood. Indication To prevent isoimmunization in Rh-negative individuals exposed to Rh-positive RBC Rh D immuno globulin micro-dose is for use only after spontaneous or induced abortion or termination of ectopic pregnancy up to and including 12 wk of gestation. Preparation Injection: single dose vial, 5% solution in prefilled syringes, 120 mcg, 300 mcg, 1000 mcg vials Usual Dose 1. Antepartum Prophylaxis Adult: IM/IV 1 vial or 300 mcg at approximately 28 wk; followed by 1 vial of mini-dose or 120 mcg within 72 h of delivery if infant is Rh-positive 2. Postpartum Prophylaxis Adult: IM/IV 1 vial or 300 mcg within 72 h of delivery if infant is Rh-positive 3. Following Amniocentesis, Miscarriage, Abortion, Ectopic Pregnancy
• 85. 85 Adult: IM 1 vial of the microdose, preferably within 3 h but at least within 72 h 4. Transfusion Accident Adult: IM/IV 1 vial or 300 mcg for each volume of RBCs infused divided by 15, given within at least 72 h of accident Contraindication Rho(D)-positive patient; person previously immunized against Rho(D) factor, hypersensitivity , severe immune globulin hypersensitivity, bleeding disorders, pregnancy , neonates, pediatric clients. Side effect Injection site irritation, slight fever, myalgia, lethargy. Nursing consideration - Obtain history of systemic allergic reactions to human immune globulin preparations prior to drug administration. - Send sample of newborn's cord blood to laboratory for cross-match and typing immediately after delivery and before administration of Rho(D) immune globulin. Confirm that mother is Rho(D) and Du -negative. Infant must be Rh-positive. Cefexime Trade name: Taxim Generic name: Cefexime Group: Cephalosporins Mechanism of action Like beta-lactam antibiotics, cefixime binds to specific penicillin-binding proteins (PBPs) located inside the bacterial cell wall, causing the inhibition of the third and last stage of bacterial cell wall synthesis. Cell lysis is then mediated by bacterial cell wall autolytic enzymes such as autolysins; it is possible that cefixime interferes with an autolysin inhibitor.
• 86. 86 Indication Effective against Streptococcus pyogenes, Streptococcus pneumoniae, and gram-negative bacilli, including Haemophilus influenzae, Branhamella catarrhalis, and Neisseria gonorrhoeae. Little activity againstStaphylococci, and no activity against Pseudomonas aeruginosa; also uncomplicated UTI, otitis media, pharyngitis, tonsillitis, and bronchitis. Preparation 200 mg, 400 mg tablets; 100 mg/5 mL suspension Usual Dose PO 400 mg/d in 1–2 divided doses Contraindication Patients with known allergy to the cephalosporin group of antibiotics. Side effect GIT: Diarrhea, loose stools, nausea, vomiting, dyspepsia, flatulence. CNS: Drug fever, headache, dizziness. Skin: Rash, pruritus, Urogenital: Vaginitis, genital pruritus. Nursing consideration - Determine previous hypersensitivity reactions to cephalosporins, penicillins, and history of other allergies - Monitor I&O rates and pattern: Nephrotoxicity occurs more frequently in patients >50 y, with impaired renal function - Report loose stools or diarrhea during drug therapy and for several weeks after. Older adult patients are especially susceptible to pseudomembranous colitis. - Take this antibiotic for the full course of treatment. - Do not miss any doses and take the doses at evenly spaced times, day and night. - Do not breast feed while taking this drug without consulting physician.