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Jaundice in Pregnancy

73

 

Rajesh Chawla and Prashant Nasa

 

A 25-year-old female at 34 weeks of pregnancy had been admitted to the hospital with jaundice for 5 days, altered mental status, and decreased urine output for 8 h. Her antenatal status was fine, with no history of pregnancy-induced hypertension. HBsAg and HIV were negative.

Jaundice in pregnancy can occur due to pregnancy-related and unrelated diseases. Pregnancy-related liver diseases are real threat to the survival of the fetus and the

mother.

Rapid diagnosis is needed to manage them appropriately.

Step 1: Initiate resuscitation

Airway intervention may be required in the following conditions:

Altered mental status and seizures.

Acute respiratory failure not responding to conservative measures.

Cesarean section under general anesthesia.

Shock – to reduce work of breathing.

Always anticipate difficult airway in pregnant patients.

Endotracheal intubation should be performed sooner rather than later to protect the airway.

Intubation must be performed by the senior intensivist.

R. Chawla, M.D., F.C.C.M. (*)

Department of Respiratory, Critical Care & Sleep Medicine, Indraprastha Apollo Hospitals, New Delhi, India

e-mail: drchawla@hotmail.com

P. Nasa, M.D., F.N.B.

Department of Critical Care Medicine, Max Superspeciality Hospital, New Delhi, India

R. Chawla and S. Todi (eds.), ICU Protocols: A stepwise approach,

585

DOI 10.1007/978-81-322-0535-7_73, © Springer India 2012

 

586

R. Chawla and P. Nasa

 

 

Difficult airway equipment for airway management must be thoroughly checked before proceeding to intubation, and the alternative plan for definitive airway including surgical access should be identified.

Raised intracranial pressure (ICP) in the jaundiced pregnant patient is a serious concern, and therefore, proper sedation should be ensured with minimal manipulation during intubation.

Supplemental oxygen may be required in some patients depending on their oxygen saturation, target SpO2 more than 95%.

Circulation

Two large-bore intravenous cannulae (14G or 16G) should be placed to administer fluids.

Be careful of associated coagulopathy.

A Foley’s catheter should be placed to monitor urine output.

Use fluid administration judiciously to optimize preload and at the same time to avoid overload, which might increase ICP.

Nurse in the left lateral position (30° wedge to the right hip) to prevent supine hypotension syndrome.

Disability (neurological)

Perform a brief neurological assessment including Glasgow coma score, pupil size, and reaction to light in case of altered mental status.

Step 2: Take history and perform physical examination

Take detailed history that should cover the following:

Details about pregnancy (trimester of pregnancy)

Antenatal evaluation and immunization

History of hypertension, pregnancy-induced hypertension during the previous pregnancy, complications and outcome of previous pregnancy, and family history of hypertension

Duration of jaundice and pruritus, other constitutional symptoms such as malaise, nausea, anorexia, fever, weight loss or increased abdominal girth from ascites, and seizures

History of abdominal surgery, medication history (amount and time of acetaminophen, herbal medications), and transfusion history

History of alcohol consumption, HIV and hepatitis risk factors, intravenous drug abuse, exposure to travel, occupational, and recreational history

History of hepatitis B or C in the spouse

In physical examination, also look for the signs of acute liver failure:

Altered mental status

Icterus, anemia

Ecchymotic patches/bleeding from gastrointestinal tract or urinary tract

Epigastric or right upper quadrant abdominal tenderness

Peripheral edema, hyperreflexia, or clonus

Seizures

73 Jaundice in Pregnancy

 

587

 

 

 

Table 73.1 Stages of hepatic encephalopathy

 

 

Stage

Mental status

 

Neuromuscular function

1

Impaired attention, irritability, depression

Tremor, incoordination, apraxia

2

Drowsiness, behavioral changes, memory

Asterixis, slowed or slurred speech, ataxia

 

impairment, sleep disturbances

 

 

3

Confusion, disorientation, somnolence,

Hypoactive reflexes, nystagmus, clonus,

 

amnesia

 

muscular rigidity

4

Stupor and coma

 

Dilated pupils and decerebrate posturing,

 

 

 

oculocephalic reflex

Table 73.2 Physiological changes in liver tests during normal pregnancy

Test

 

Normal range

Bilirubin

Unchanged or slightly decreased

Aminotransferases

Unchanged

Prothrombin time

Unchanged

Alkaline phosphatase

Increases two to four fold

Fibrinogen

Increases by 50%

Triglycerides

Increases

Globulin

Increases in a- and b-globulins

 

 

Decreases in gamma globulin

Cholesterol

Increases twofold

Hemoglobin

Decreases in later pregnancy

WBC

 

Increases

Hypotension (hypovolemia, hemolysis, sepsis)

Spider angioma and palmar erythema may be normal in pregnancy

Step 3: Assess the severity of hepatic encephalopathy

One should assess the severity of hepatic encephalopathy to plan the appropriate treatment (Table 73.1).

Step 4: Send investigations

Complete blood cell count.

Liver function tests—remember normal physiological changes in pregnancy (Table 73.2).

Renal function tests and serum electrolytes.

Arterial blood gas analysis and blood glucose.

Hepatotropic virus profile (IgM anti-HEV, IgM anti-HAV, IgM anti-HCV, antiHBc antibody, HBeAg, HBsAg).

Coagulation profile (prothrombin time, activated partial thromboplastin time, fibrinogen, fibrin degradation product).

Uric acid.

The antinuclear factor—to exclude autoimmune hepatitis.

Additional tests—peripheral smear, serum lactate dehydrogenase levels, reticulocyte count, and Coombs’ test—to exclude thrombotic thrombocytopenic purpura (TTP).

588

 

R. Chawla and P. Nasa

 

 

Table 73.3 Classification of liver diseases in pregnancy

 

 

Pregnancy-unrelated liver diseases

 

 

Liver diseases coincident

Pregnancy-related liver diseases

Preexisting liver diseases

with pregnancy

Intrahepatic cholestasis of pregnancy

Hepatitis B and C

Biliary disease

(ICP)

 

 

Preeclampsia and eclampsia

Autoimmune liver disease

Budd–Chiari syndrome

Hemolysis, elevated liver enzymes,

Wilson’s disease

Drug-induced

low platelet (HELLP) syndrome

 

hepatotoxicity

Acute fatty liver of pregnancy (AFLP)

Cirrhosis and portal

Viral hepatitis A and E

 

hypertension

 

Hyperemesis gravidarum

 

 

Ultrasonography is considered safe and is the preferred abdominal imaging modality during pregnancy.

MRI with contrast is preferable to CT scanning during pregnancy to avoid ionizing radiation.

Transthoracic echocardiography.

Step 5: Differential diagnosis

The various conditions that can cause acute hepatic failure can be divided into those related to pregnancy and those unrelated to pregnancy (Tables 73.3 and 73.4).

A.Hyperemesis gravidarum

Incidence: 0.3–2.0% of all pregnancies.

Usually within the first trimester.

Symptoms: intractable vomiting, resulting in dehydration, ketosis, and weight loss of 5% or more.

The cause remains unclear.

Risk factors: obesity, psychiatric illness, molar pregnancy, preexisting diabetes, multiple pregnancies, and hyperthyroidism (60%).

Serum aminotransferases can rise up to 20 times, but jaundice is rare.

B.Viral hepatitis

Diagnosis of viral hepatitis in pregnancy is not different from the diagnosis in the nonpregnant state.

Herpes simplex virus in patients who are immunosuppressed, and in the pregnant woman, can cause fulminant hepatitis. Aminotransferases are high, and other signs of hepatic failure such as prothrombin time are elevated, but jaundice (increase in bilirubin) is rare.

Step 6: Management

A.AFLP

Prompt delivery is essential (steroids if fetal maturity in doubt).

Supportive treatment, control of hypertension (discussed in Chap. 19), and correction of coagulation abnormalities and hypoglycemia.

Table 73.4 Comparison of severe preeclampsia–eclampsia, intrahepatic cholestasis of pregnancy, HELLP syndrome, and AFLP

 

Severe

Intrahepatic cholestasis

 

 

 

preeclampsia–eclampsia

of pregnancy

HELLP syndrome

AFLP

Trimester

Second to third

Second to third

Third

Third

Incidence (%)

1–5

0.1

0.2–0.6

0.005–0.01

Family history

Occasionally

Often

No

Occasionally

Presence of preeclampsia

Yes

No

Yes

50%

Typical clinical features

Hypertension, edema,

Pruritus, mild jaundice,

Hemolysis

Liver failure with coagulopathy,

 

proteinuria, neurological

elevated bile acids

Thrombocytopenia (<50,000

encephalopathy, hypoglycemia,

 

deficits (headaches, seizures,

 

often)

disseminated intravascular coagulation

 

coma)

 

 

 

Aminotransferases

None/mild

Mild to 10to 20-fold

Mild to 10to 20-fold

300–500 typical but variable ++

 

 

elevation

elevation

 

Bilirubin

Normal— <5 mg/dL

<5 mg/dL

<5 mg/dL unless massive

Often <5 mg/dL, higher if severe

 

 

 

necrosis

 

Hepatic imaging

Normal—hepatic infarcts

Normal

Hepatic infarcts hematomas,

Fatty infiltration

 

 

 

rupture

 

Histology (usually not

Periportal hemorrhage,

Normal–mild cholesta-

Patchy/extensive necrosis

Microvesicular fat in zone 3

performed)

necrosis, fibrin deposits

sis, no necrosis

and hemorrhage

 

Recurrence in subsequent

20% risk

45–70%

4–19%

Subunit, long-chain 3-hydroxyacyl-

pregnancies

 

 

 

CoA dehydrogenase defect—yes

 

 

 

 

No fatty acid oxidation defect—rare

Pregnancy in Jaundice 73

589

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