Table 9-1. Pregnancy Induced Hypertension (PIH)



  Mild PIH Severe PIH Eclampsia  
Symptoms None Headache or Unexplained convulsions  
    epigastric pain or    
    visual changes    
         
Sustained >140/90 mm Hg At least >140/90 (if At least >140/90 mm Hg  
↑ blood pressure <160/110 mm Hg other findings) or    
    >160/110 mm Hg    
         
Laboratory tests Hemoconcentration Hemoconcentration Hemoconcentration  
  >300 mg proteinuria > 5g proteinuria in At least 1-2 +  
  in 24 hrs 24 hrs or DIC, or proteinuria  
 

No DIC, normal liver

↑ liver function tests    
       
  function tests      
         
Other findings None Pulmonary edema May or may not be  
    oliguria, cyanosis present  
         
Management <36 wk: observe in

MgSO4: prevent or treat convulsions

 
  hospital, no MgSO4,

Lower diastolic BP to 90–100 mm Hg

 
  or blood pressure

Prompt delivery: not necessarily Cesarean

 
 

meds

 
 

section

   
       
  >36 wks: prompt      
  delivery      
         

OB Triad


 

CHRONIC HYPERTENSION WITH OR WITHOUT SUPERIMPOSED PREECLAMPSIA

 

A 35-year-old multigravida is seen in the outpatient prenatal clinic for her first prenatal visit. She is at 12 weeks’ gestation with a BP of 155/95. Chronic hypertension was diagnosed 5 years ago for which she has been treated with oral nifedipine. A spot urine dipstick protein is 2+. A recent 24-h urine collection showed

 

1.2 g of protein and a creatinine clearance of 85 ml/min. Serum creatinine is 1.2 mg/dl. She has no complaints of headache or visual changes.


 

Chronic HTN

 

• Pregnancy <20 wk or prepregnancy

• Sustained HTN (>140/90 mm Hg)

• +/– proteinuria


 

Risk Factors. Most chronic hypertension (HTN) is idiopathic without specific antecedents.Risk factors are obesity, advanced maternal age, positive family history, renal disease, diabetes, and systemic lupus erythematosus.

 

Etiology/Pathophysiology. Pathophysiology is vasospasm causing decreased end-organ perfu-sion, resulting in injury and damage. The acute problems arise from excessive systolic pressures,whereas the long-term problems arise from excessive diastolic pressures.

 

Diagnosis. The diagnosis of chronic HTN is made when BP≥140/90 mm Hg with onset beforethe pregnancy or before 20 weeks’ gestation.

 

 

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USMLE Step 2 l Obstetrics

 

 

Pregnancy Prognosis with Chronic HTN:

Good. Favorable maternal and neonatal outcome is found when BP 140/90–179/109 mm Hg and no evidence of end-organ damage.

 

Poor. Pregnancy complications are more common in patients with severe HTN withthe following end-organ damage: cardiac, renal, and retinal.

 

Renal disease. Pregnancy loss rates increase significantly if serum creatinine value are >1.4 mg/dL.

 

Retinopathy. Longstanding HTN is associated with retinal vascular changes including hemorrhages, exudates, and narrowing.

 

Left ventricular hypertrophy. This is seen mostly in women with prolonged BP values >180/110 mm Hg.

 

Worst. Tenfold higher fetal loss rate if uncontrolled HTN (before conception or earlyin pregnancy) and chronic HTN with superimposed preeclampsia.


 

OB Triad

Chronic HTN with Superimposed Preeclampsia

• Chronic HTN

 

• Worsening BP

 

• Worsening proteinuria


Chronic HTN with Superimposed Preeclampsia:

 

• This complication occurs in 25% of patients with chronic HTN. Risk factors include renal insufficiency, HTN for previous 4+ years, and HTN in a previous pregnancy.

 

• Adverse pregnancy outcomes for both mother and baby are markedly increased.

 

Abruptio placenta incidence is markedly increased.

 

• The diagnosis is made on the basis of established chronic HTN along with any of the following: documented rising BP values; demonstrated worsening proteinuria; or evidence of maternal jeopardy (headache, epigastric pain, visual changes, thrombo-cytopenia [platelet count <100,000/mL], elevated liver enzymes, pulmonary edema, oliguria [<750 mL/24 h], or cyanosis). Edema may or may not be seen.


 

Laboratory Abnormalities. Chronic HTN patients have a spectrum of etiologies and diseaseseverity. Those with mild HTN and no end-organ involvement have normal laboratory tests, whereas those with renal disease may have evidence of decreased renal function including pro-teinuria, lowered creatinine clearance, and elevated BUN, creatinine, and uric acid.

 


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