Author Information
Asmita Patil*, Parulekar SV**, Samant PY***.
(*Senior
Resident, ** Professor and Head of Department, *** Associate Professor. Department of Obstetrics and Gynecology, Seth G. S. Medical College & K.E.M. Hospital ,
Mumbai , India
Abstract
Among the
complications of eclampsia, Hemolysis Elevated Liver enzymes Low Platelets
(HELLP) syndrome figures prominently as a cause of aggregated morbidity and of
mortality. It is an important complication of pregnancy, and it typically
happens in women with known diagnosis of pre-eclampsia.[1]
Neurological complications of eclampsia include mental confusion, seizures,
cortical blindness, deficits in the visual fields. At neuroimaging,
abnormalities includes cortical edema, intracerebral hemorrhage and Posterior
Reversible Encephalopathy Syndrome(PRES).[2] Here we present a case
of late onset HELLP syndrome with postpartum eclampsia complicated with PRES.
Introduction
Preeclampsia
and eclampsia are two clinical situations that are exclusively associated with
pregnancy. Symptoms typically begin after the 24th week of
pregnancy. Pre-eclampsia and eclampsia figure among the three most important
causes of death in pregnancy.[2]
Pre-eclampsia
and eclampsia can have many serious complications; among them HELLP syndrome
and PRES are two separate entities but very rarely they can present concurrently.
We describe a case of association between HELLP syndrome and PRES in a patient
with postpartum eclampsia. This association is poorly described. Very few cases
have been reported till today.[3-6]
Case Report
A 25 year old female G2P1L1
with 9 months amenorrhea presented with pain in abdomen since 5 to 6 hours and
gestational hypertention first time diagnosed on admission. Her blood pressure
was 140/90 mm Hg and proteinuria of 4+. She had no premonitory symptoms. Her
deep tendon reflexes were normal. She was given Tab. Alfa methyldopa 250 mg 8
hourly and Cap.Nifedipine 5mg orally as required. She was in active labor, and
delivered a live1.7 kg female baby vaginally within 30 minutes. Two hours postpartum
her B.P. was 130/90 mm Hg and proteinuria reduced to 2+. Her renal chemistry
and liver function tests reports were within normal limits. After 12 hours
patient was found slightly icteric and pale. Her blood pressure was 160/100 mm
of Hg, urine albumin 2+ and deep tendon reflexes were normal, she had no
premonitory symptoms; hence the dose of antihypertensives was increased, Tab.
Alpha methyldopa 6 hrly and C. Nifedepin 10 mg 6hrly. Her PIH profile was sent
again. Which came as, Hb 13.1gm% , WBC: 10000/cmm, platelets 56000/cmm,
INR:1.25, P.T :16.5sec, control :13.5sec, total bilirubin 3.4mg/dL, direct
bilirubin 1.5mg/dL, SGOT:520U/L, SGPT :362U/L, lactic dehydrogenase240U/L.
Renal function test, serum electrolytes, plasma proteins were within normal
limits. Viral markers for hepatitis A,C,B,E were negative. A diagnosis of HELLP
syndrome was made; physician reference was done, they advised Injection
Cefotaxime , Injection Metronidazole and
I.V. fluids to be given. 24 Hrs later icterus was profound, blood pressure was
in the range of 150/90 mm Hg and hematuria was present. Her repeat
investigations showed deranged coagulation; PT : 10.8 sec., control: 8.9 sec, INR :1.21, PTT Test:31.0 sec, control: 29 sec, thrombin time: 15, fibrinogen: 334, FDP:>320
(N-<5), D-Dimer: >10(N-<0.3 mg/L). As per Haemotology reference 4
units platelet transfusion was given, 35 hrs later patient had gereralized tonic clonic seizures. Blood pressure:
150/100 mm Hg, Proteinuria- 2+, Deep tendon reflexes were normal. Inj.MGSO4
by ZUSPAN regime was started and antihypertensives were continued.
Physician reference taken again advised Inj. Phenytoin sodium 100 mg stat and
then twice a day , 4 units of platelets transfusion & transfer to Medical Intensive
Care Unit(ICU) .Computed Tomography brain done, showed posterior reversible
encephalopathy syndrome. IV antibiotics, Inj.mannitol and antihypertensives
given in Medical ICU; patient recovered completely over a period of 5 days.
Discussion
HELLP
syndrome is rare before the 20th week of pregnancy. In 1/3rd
of the cases it happens in the immediate post-natal phase. Hematologic (DIC)
and cardiopulmonary events (pulmonary edema, acute cardiac insufficiency) are
commonly observed. Neurological alterations (cerebral bleeding,
hypoxic-ischemic encephalopathy) are seen in only 4.5% of patients.[7]
Feske et
al. showed that endothelial dysfunction is likely important cause in the
genesis of the syndrome. The endothelium would be directly damaged by factors
such as vasospasm, ischemia, platelet activation, increase in the levels of
vasoactive molecules such as serotonin and thromboxane A-2, activation of the
coagulation system, and impairment in the action of the normal placentally
mediated adaptations to prostacyclin , nitrous oxide, as well other endothelial
mediators of the vascular tone and of vascular permeability. Hinchey etal. also
has described that, the vasoactive
mechanism, with damage and loss of the cerebral vascular auto regulation, is
the proposed basic mechanism for PRES.[8] The clinical observation
that the vascular system in the anterior regions of the brain have more dense
sympathetic innervations, as compared to the posterior regions, which may
explain the predilection for edema in the posterior regions of the brain,
especially in the parieto- occipital regions.[9-11]
In this
article we have reported a rare association between HELLP syndrome , PRES and
eclampsia of late onset. It seems that endothelial vasogenic mechanisms led to
the neurologic manifestations which occurred in our case. The effective and
fast correction of the blood pressure levels, associated to the quick
recognition and treatment of the HELLP
syndrome and PRESS resulted into good outcome.
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Citation