Preeclampsia and Eclampsia: Diagnosis and Management

Introduction

Preeclampsia is termed as hypertension that occurs during pregnancy usually after the 20th week of gestation. Preeclampsia is characterized by an elevated blood pressure (hypertension) and presence of proteins in urine (proteinuria). It usually presents between the second and third trimesters even though some studies show that it can present at any time during pregnancy. The main method thought to lead to complete remission is giving birth and final removal of the placenta. Preeclampsia is believed to be a result of a myriad of factors. These can be of maternal, foetal or placental origin.

Defects in the development and functioning of the placental blood vessels are a major cause of preeclampsia. The defective blood vessels result in decreased blood flow to the affected area. As a result, the blood vessels respond by releasing factors that may interfere with the normal functioning of blood vessels themselves resulting in precipitation of a hypertensive situation. The arteries supplying the placenta may develop a defect such that they transform themselves from being the low capacity strong vessels to high capacity vessels with diminished opposition to blood flow. As a result the amount of blood delivered to the placenta becomes more and the placenta cannot handle the volume. This in turn brings about the hypertension observed in pregnancy. In addition, an abnormality during the differentiation of the trophoblast has been cited to one of the causes of preeclampsia. THIS BRINGS ABOUT formation of an impaired placenta that in turn precipitates the development of preeclampsia. Immunologic factors also play a role in the precipitation and pathogenesis of preeclampsia. Pressure to the placental is perceived to be foreign resulting in production of defence immunologic factors. These factors in turn prime the placenta resulting in morphologic changes within the placental wall. An elevation in the sensitivity of the placenta to various hormonal mediators has also been cited as a major factor involved in pathogenesis of preeclampsia. Researchers have linked this to the amplification of the amount of B2 bradykinin receptors present within he placental walls of women with preeclampsia. These receptors mimic the angiotensin two receptors resulting in increased stimulation of the placental wall and as such precipitating hypertension during pregnancy. If not well managed, preeclampsia may be fatal. At times the presentation of preeclampsia may be masked by other conditions making definitive diagnosis difficult. The management of expectant mothers is a multidisciplinary undertaking that involves every member of the medical team to achieve the desired goals.

Clinical Presentation and Examination

A 29-year-old primigravid woman weighing 80 kg presented to the labour ward from home, at 37 weeks with one week’s history of visual disturbances and headache. In addition, she complained of epigastric pain and oedema of the lower extremities. At the hospital, the patient had an episode of seizure that lasted for around 30 seconds. The patient was admitted to the ward for further review. At the labour ward the blood pressure was immediately taken and the patient had an elevated blood pressure with systolic pressure at 160mmHg while the diastolic pressure was at 112mmHg. Analysis of the urine using a dipstick showed an elevated level of protein in urine. The presumptive diagnosis made was that of preeclampsia.

The care setting of the hospital comprises of a labour and delivery unit. In addition there is a high dependency unit that provides for maintenance of patients in critical condition. In addition, it has a side lab for expedited laboratory measurements. The nurse present was requested to obtain the patient’s blood pressure. This was carried out by placing the cuff at the level of the heart with diastolic readings being inferred from the abolition of heart sounds. It was found out that she had a systolic blood pressure of 180mmHg and a diastolic pressure of 110mmHg. Laboratory tests revealed that she had 0.5g of proteins in her urine and there was marked thrombocytopenia together with deranged liver function. Based on these measurements the patient was classified to have severe preeclampsia and as such the severe preeclampsia protocol was initiated. Other laboratory tests carried out confirmed the diagnosis. These included an elevated aspartate aminotransferase AST level and a low platelet count. Since the patient was in a lot of pain the team put him on 50mg of pethidine and 12.5 mg 0f 12.5mg prochlorperazine to ensure monitoring of the patient was carried with minimum interference.

Multidisciplinary Team Approach

The attending nurse transferred the patient to a spacious room within the labour ward. She then made a call to the attending obstetrician explaining the situation at hand. After that she made a call to the anaesthetist and a registrar specializing in obstetric medicine and informed them of the same and requested their presence. An intensive care observation chart was obtained and monitoring initiated to ensure constant monitoring of the patient. The patient was then transferred to the high dependency unit. The chart consists of the basic personal information, vital signs and the updated status of the patient. Monitoring was initiated with immediate effect. Blood was then drawn from the patient for a battery of tests. The blood was taken to the laboratory for measurement of the full blood count (FBC), Urea, Electrolyte and Creatinine (UEC) and the liver function tests (LFT). Other lab tests were requested. These included platelet level, amount of uric acid present, and cross matching of the blood groups just in case the patient needed a transfusion after admission. Other tests such as the coagulation screen were ordered for. Urine was collected and taken to the lab for a compressive microscopic analysis. In addition, there was a request for culturing the urine and sensitivity assay. Since there was an initial suspicion of HELLP (haemolysis, elevated liver enzymes, low platelets) syndrome blood film was requested for further analysis. Serum glucose was determined using a glucometer and the results recorded. At one hour after checking in at the ward, most of the parameters were within normal ranges except for the blood pressure which was still high.

For a period of over four hours both maternal and foetal parameters were within normal limits when with a sudden onset the foetal heart rate fell below 90 beats per minute for about two and a half minutes. The team initiated a rapid intervention by trying to adjust the position of the foetus to a lateral one and using a facemask to deliver oxygen. Vaginal review revealed intact membranes. The team decided to go ahead and create an artificial rupture. The team then decided to move the patient to the theatre for an emergency operation. This was due to the assumption of placental obstruction resulting in decrease in foetal blood pressure. The team decided on performing an emergency caesarean operation. The anaesthetist administered 30mL of sodium citrate to the patient orally. The strength of the sodium citrate used was 0.3M. Rapid sequence induction with pre-oxygenation and cricoid pressure, thiopentone 450 mg, suxamethonium 100 mg and intubation with a cuffed endotracheal tube was followed by maintenance with an oxygen 50% and nitrous oxide 50% mixture and isoflurane 1%. Analgesia was provided with alfentanil 750 lg.

The procedure went on smoothly and a kicking male infant was delivered. The infant weighed approximately three and a half kilograms. Apgar scores were 4 at 1 min, 8 at 5 min and 9 at 10 min. The pH of the umbilical artery was slightly acidic at a value of 6.213. This necessitated administration of morphine 15 mg and Syntocinon 10 IU to reduce pain associated with the operation. The overall blood loss was estimated at 500mL and the patient was subjected to a fluid challenge by administration of approximately 200mL of Gelofusine and 6g of ephedrine to counter the hypotension. As a result, there was an increase in the heart rate to about 108 beats per minute. However, there was little change in the blood pressure. Methoxamine was then administered at a dosage of 2mg and this elevates the systolic blood pressure to an average of 116mmHg. The oximeter revealed sufficient oxygenation at aboutb100%. The mother and the infant were maintained in the delivery room for a period of about four hours. During this time both parties were stable with the maternal blood pressure ranging from 112mmHg to about 138mmHg. The maternal heart rate was between 65 to 90 beats per minute. The urine over this period of time was 120mL. A patient controlled analgesia (PCA) was provided to the patient for management of post operative pain. The PCA contained neat morphine at a concentration 1mg/mL. At about five hours post operation the patient developed a tachycardia of about 120 beats per minute with a very low blood pressure of about 80mmHg/60mmHg. Consequently, the colour of urine darkened and there was a marked decrease in urine output to about10mL per hour. The medical team decided to initiate a by administering 250nl of Gelofusine but they observed very little change in the blood pressure. The urine output decreased even further to about 5mL per hour. The lab results of blood analysis revealed a decrease in the haemoglobin concentration to about to 7.6 g/dL. There was marked thrombocytopenia with deranged values for the coagulation screen. Another fluid challenge was initiated with no improvement in the heart rate. At this juncture, the medical team concluded that the patient was suffering from disseminated intravascular coagulation (DIC). After 7 hours urinalysis revealed increase in urea, and creatinine levels. The patient was then put under review by the anaesthetist to ascertain the cause of the manifestations. Further review showed that the patient had jaundice and the colour of the urine was darkening to the point of almost being black.

Consequently, a repeat of the blood studies showed a marked thrombocytopenia with a marked reduction in the haemoglobin level to about 3.9g/dL. In addition, the patient was becoming more hypotensive with time. The team did not know whether the observed clinical picture was due to haemolysis or haemorrhage. To rule out haemorrhage, the team decided to carry out an abdominal ultrasound. The results of the ultrasound showed absence of unusual fluid and this enabled the team to rule out haemorrhage as the cause of the observed clinical picture. Further tests were carried out Thromboelastography (TEGs) revealed a straight demarcation an indicator of complete failure of the coagulation process most probably due to absence of a [particular clotting Factor. As a form of intervention, Fresh Frozen Plasma (FFP) was given to the patient, since the findings pointed to a working diagnosis of HELLP (haemolysis, elevated liver enzymes, low platelets). The intervention consisted of administration of four units of FFP and 12 units of platelets. In addition, a diuretic in this case furesimide 40mg was administered in conjunction with two units of packed red cell. At nine hours post partum, Thromboelastography (TEGs) revealed a slight improvement in the coagulation profile and another round of FFP was given to facilitate improvement of the clot initiation process. A central vein was canulated for administration of desmopressin (DDAVPsR) and nacetylcysteine. At eleven hour s post partum the cardiovascular system was functioning at optimum and the patient was stable. The systolic blood pressure was between 135mmHg and 150mmHg.

Consequently, the heart rate was at around 106 meats per minute. Other parameters such as oxygen saturation and central venous pressure were within normal ranges. Repeat TEGs, showed formation of a better clot implying that the amount of factors administered were adequate. At around fifteen hours post partum the patient was stable save for diastolic hypertension. 200mfg of labetalol was administered to mange the hypertension. However at 17 hours post partum, the patient’s condition worsened. Laboratory tests showed a marked increase in various parameters. Urea creatinine and the liver function tests were markedly elevated the alanine aminotransferase (ALT) and alkaline phosphatise were markedly elevated. Markers of the liver function such as bilirubin were deranged indicating possible damage to the liver. The renal unit team was called in to review the patient. They immediately suggested that the patient should be moved to the high dependency unit for dialysis. The patient was wheeled from the labour ward to the high dependency unit. At this time the patient was maintained on respiratory support using a facial CPAP. The patient was then infused with GTN to ensure tat the cardiovascular system was not overloaded. However, immediately after commencement of GTN infusion, the patient went into a hypotensive state necessitating the administration of epinephrine. After this the patient developed ventricular tachycardia and this required administration of 50mg of lidocaine and 20 mmol magnesium. This ensured that the patient was stable enough to be taken through the dialysis process. At around 25 hours post operative, the process of dialysis was initiated and continued for a further three hours. This resulted in removal of about four litres of fluid. Due to the risk of excessive bleeding, heparin was not administered and instead prostacyclin was given. The patient remained in the high dependency unit for a total of 18 hours after which she was transferred to the renal unit for further sessions of dialysis. After a total of nine days, the patient was allowed to go home with her baby.

Anti-Hypertensive Therapy

Anti-hypertensive therapy was initiated immediately to prevent precipitation of stroke by the high blood pressure. Intravenous therapy is preferred for quicker but safe reduction of blood pressure to tolerable levels.

Hydralazine

Hydralazine was administered at an intravenous bolus dosage of 5 mg over a period of five minutes. Blood pressure was taken after that using the automated blood pressure machine. The diastolic pressure was found to be still elevated. The procedure was repeated after 20 minutes until the diastolic blood pressure was below 100mmHg. Maintenance therapy was initiated by use of a continuous infusion method that employed a syringe containing 60 mg of hydralazine in 60mL of 0.9% sodium chloride. The rate of infusion was maintained at the rate of 5mL/hr 5 mg/hr and as time went it was titrated against the expectant mother’s mean arterial blood pressure with a target of mean arterial blood pressure of less than 125mmHg and a diastolic blood pressure of less than 100mmHg. It was observed that the blood pressure was rising again during this period. This necessitated administration of 5mg of sublingual nifedipine to ensure there was a tight control on the blood pressure.

Magnesium Sulphate

A Bolus dose of 4 g Magnesium Sulphate was administered intravenously over a period of five minutes to control the seizures. This was achieved through administration of 20mL of the 20% magnesium sulphate solution. The patient was then started on a maintenance dose by use of a syringe pump containing12 g of magnesium sulphate. The infusion was run at the rate of 5mL/hr which translates to 1g/hr. Monitoring was done by checking on the tendon reflexes immediately after administration of the loading dose. Thereafter, monitoring is carried out on hourly basis. In addition, respiratory rate was monitored hourly in addition to checking on the level of consciousness of the patient at the rate of every hour. During the infusion process, it was observed that the urine output fell below 50mL in a period of 2 hours. The specialist obstetrician was immediately called by the attending nurse. The specialist ordered the cessation of the maintenance infusion. The anaesthetist was informed and blood drawn to determine the amount of magnesium in the blood steam. 1 g of calcium gluconate was administered intravenously over a period of 3 minutes to counter the toxic effects of magnesium sulphate on the heart. The patient was stabilized and the respiratory rate returned to normal.

Monitoring

An input output chart was started for strict monitoring of the fluid intake and output. This was necessary to prevent worsening of the condition by limiting the fluid burden on the already burdened heart. Consequently, urine output chart was provided to monitor the amount of urine. Monitoring was carried out ant intervals of one hour to ensure the patient remained stable. Blood Pressure monitoring was carried out y obtaining measurements every 15 minutes utilizing automated blood pressure recorder. The procedure was repeated manually after an hour using a sphignomanometer and stethoscope. One hour into checking in at the facility, the pulse oximetry exhibited an oxygen saturation of about 97%, while the urine output was above 30mL though the urine had trace amounts of blood visible to the naked eye. The results from the laboratory tests showed a slight elevation in liver function tests especially with the alanine aminotransferase (ALT) and alkaline phosphatise. There was slight thrombocytopenia further confirming the diagnosis of preeclampsia.

The Role of the Midwife in Preeclampsia management

The midwife is involved in the care of the expectant mother both in the pre and post natal periods. The midwife plays an important role in the management of expectant mothers to prevent development of complications through programmed monitoring procedures. Whether be it in the labour ward or in the high dependency unit, the role of the mid wife is undisputed. In this case scenario the midwife monitored the patient’s airway condition through recording of the respiratory parameters on a predesigned chart. The oxygen saturation of the patient had fallen below the required level and is the midwife who informed the anaesthetic and the senior specialist registrar to consider admitting the patient to the high dependency unit. The midwife was also involved in the airway condition monitoring that entailed monitoring of the level of oxygen saturation. The midwife maintained ITU charts at an interval of one hour. These charts included the fluid input and output charts, urine output chart, the blood pressure chart. Others included the central venous pressure and oxygen charts. Other important occurrences were filled in special charts. These included the delivery time, epidural insertion time and the pharmacological intervention charts that included the dose and time of administration of the antihypertensive medications. In addition, the amount of blood lost during delivery was recorded.

The midwife carried out blood pressure measurements with the help of an assisting midwife. This was carried out at interval s of 15 minutes using an automated blood pressure machine. The procedure was repeated at intervals of one hour manually using a sphignomanometer and stethoscope. The midwife took two readings which are the mean arterial pulse and the diastolic pressure and relayed the information to the specialist registrar in cases where the mean arterial pressure rose beyond the 125mmHg on more than one occasion.

The midwife monitored the fluid intake including the fluid contained in any drug infusions. She maintained the hourly fluid intake intravenously at the rate of 85mL/hr. Al the readings were recorded on the fluid intake chart and any adjustments were also recorded. She monitored the urine output by use of an urimeter. She updated the obstetrician of the state of the patient in terms of urine output. The midwife monitored the infusion of the magnesium sulphate for any signs of toxicity. Monitoring was carried out by checking on the tendon reflex and the state of respiration.

Conclusion

Preeclampsia and other conditions that occur in pregnancy may be life threatening if there is lack of proper diagnosis and timely intervention. From the case report, the patient had a bout of haemolyses. This ties the diagnosis to HELLP. HELLP has more deleterious effects when compared to preeclampsia and may result in death of the patient if not adequately managed. Even though, it was evident that there was co morbidity of preeclampsia and HELLP (haemolysis, elevated liver enzymes, low platelets), it took the junior staff a longer time to report it to the more experienced specialist. However after the diagnosis was made there was an expedited process of intervention that resulted in saving the life of the mother and the baby. In preeclampsia, there is always a hurdle in the way fluids are managed. This stems from the fact that in preeclampsia there is increased resistance to circulation of the fluids within the vascular r compartment. In addition, there is a tendency of the body to inadequately control of the incoming fluid resulting in elevated blood pressure since the heart is under immense stress to push the colloidal fluid through the system. If poorly managed, preeclampsia may result in precipitation of pulmonary oedema which leads to laboured pain and resulting in provision of respiratory support to the patient. Since the patient developed anaemia, there was a need to carry out blood transfusion. In addition, the [presence disseminated intravascular clotting (DIC) there was a need to initiate management through the provision of FFP to the patient. Since there was a haemolytic process, there was excessive breakdown of haemoglobin and this may have resulted in the acute renal failure picture observed. Of concern was the repletion of the challenge on the kidney with fluids despite the clinician’s knowledge of the danger of a haemolytic process on the kidney function. The kidneys were already overworked and there was no need to challenge it. Laboratory testes should have been used more to determine the course of the clinical picture. As an example, the clinicians should have relied more on TEGsR to determine the course of the transfusion process.

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