headache for all…

The Case.

A 28 year old female presents to your ED at 2am. She left the hospital 12 hours earlier with her newborn first child who is now 2 and half days old. Her main complaint is that of profound lethargy, fatigue, severe worsening bifrontal headache and breathlessness.

She is normally fit and well, takes no regular medications & has no significant past medical history. Her pregnancy was uneventful, but her delivery (at 39 weeks) was slightly hair-raising with foetal distress & decelerations due to an obstructive labour (requiring a ventouse).

She looks lethargic and is laying quietly in bed, but is speaking in full sentences. Her observations are within normal limits, but her BP catches your eye at 154/89. Her cardiorespiratory exam is unremarkable (specifically, her chest is clear, there are no murmurs & I cannot see a JVP). Her belly is soft with a palpable uterus, midway between  umbilicus & pubic symphysis. She has no peripheral oedema. Her GCS is 15 with reactive pupils and normal cranial nerves. She has impressively brisk reflexes (you don’t need your tendon hammer) and her power/tone/sensation appear symmetrical & normal.

Her bloods are completely normal! (FBC, LFTs, PLTs, even the CRP) !!

Now what ??

I was stumped & my differentials were far & wide. I basically documented the following…

  • Headache, hypertension, pregnancy…
    • ?Post-Partum Pre-Eclampsia
  • Weakness, lethargy, dyspnoea…
    • ?Peri-partum Cardiomyopathy
  • Headache (recent pregnancy)
    • Cerebral venous sinus thrombosis
  • Was she just depressed ???

The Continuation.

She is admitted under Obstetrics for “observation” and by morning was receiving hydralazine & labetalol after her BP climbed to the 190-220mmHg systolic range, with ongoing severe headache. 

CT-Brain w/ contrast ruled out cerebral sinus thrombosis & an MRI showed no sign of hypertensive encephalopathy (PRES).

Her LFTs, PLTS & Hb remained normal during her admission.

Pre-Eclampsia

Hypertension occurs in ~6-8% of all pregnancies.

Definitions:

  • Gestational hypertension (new BP > 140/90 mmHg) occurs during pregnancy (>20 weeks gestation) and resolves in the postpartum period (within 3 months of delivery).
  • Preeclampsia is gestational hypertension plus proteinuria (>300mg in 24 hours or 1+ protein on 2 separate urinalyses within 4-6 hours).
      • Regarded as severe if in the presence of multiorgan involvement.
  • Eclampsia is the occurrence of seizures in a patient with signs of preeclampsia.

Pre-eclampsia is the commonest medical complication of pregnancy & is associated with substantial morbidity and mortality for both mother and baby. It is a multisystem disorder of unknown aetiology that is unique to human pregnancy and is characterised by an abnormal vascular response that is associated with increased systemic vascular resistance, enhanced platelet aggregation, activation of the coagulation system, and endothelial-cell dysfunction.

Risk factors for the development of preeclampsia include; advanced maternal age, previous preeclampsia, obesity, multiple pregnancies, preexisting thrombophilia (Factor V Leiden, Protein C or S deficiency, homocysteinaemia etc) & limited exposure to father’s sperm.

Complications:

  • CNS
    • Eclampsia (seizures)
    • Cerebral haemorrhage or oedema
    • Cortical blindness
    • Retinal oedema
    • Retinal blindness / ischaemia
  • Renal
    • Cortical or tubular necrosis
  • Respiratory
    • Laryngeal oedema
    • Pulmonary oedema
  • Liver
    • Jaundice
    • HELLP syndrome
        • Haemolysis
        • Elevated LFTs
        • Low PLTs
    • Hepatic haemorrhage or rupture
  • Haematological
    • Disseminated intravascular coagulopathy
    • Microangiopathic haemolysis
  • Placenta
    • Infarct or abruption
  • Foetus
    • Preterm delivery
    • Intrauterine growth retardation
    • Hypoxia / neurological sequelae
    • Periterm death

Clinical Features:

  • Severe hypertension (systolic > 160mmHg or diastolic > 110 mmHg)
  • Persistent &/or severe headache
  • New epigastric pain & tenderness
  • Vomiting
  • Visual disturbances (blurred vision, photophobia, diplopia, scotomata & cortical blindness)
  • Hyperreflexia (brisk deep tendon reflexes)
  • Oliguria
  • Dyspnoea or retrosternal chest pain
  • New swelling to hands, face or feet.

Investigations:

  • Raised serum creatinine
  • Thrombocytopenia (PLTs < 100)
  • Evidence of haemolysis (elevated Bilirubin or low haptoglobins)
  • Haemoconcentration
  • Deranged LFTs (2x upper limit of normal)
  • Urinalysis: 1+ protein, >300mg / 24hours.
  • CT-Brain: ?intracerebral haemorrhage (patchy haemorrhages & micro-infarcts can occur) ?sinus thrombosis

Management:

The textbook answer lies with adequate and proper prenatal care & monitoring, including identification of women at high risk, early detection by the recognition of clinical signs and symptoms, and progression of the condition to severe state.

Whilst the only definitive ‘cure’ is delivery (which is always appropriate for the mother), it might not be best for a very premature foetus. The decision between delivery and expectant management depends on fetal gestational age, foetal status and severity of maternal condition at time of assessment.

From an Emergency Department perspective, it involves early identification of the disease with prompt referral to Obstetrics.


** Figure taken from Lancet 2005; 365: 785–99 **

For the ED doc, it is important to know the following;

  • Suspect & find evidence of end-organ dysfunction
  • Control blood pressure (aim diastolic BP <105 mmHg)
      • Methyldopa & CCBs for long term therapy
      • Hydralazine (5-10mg IV q20min)
      • Labetalol & Nimodipine also appropriate
      • Avoid beta-blockers (esp. Atenolol), ACEi & ARBs.
  • Control seizures
      • Magnesium sulfate:
          • 4-6 grams loading, then 2g/hr infusion
          • Observe for respiratory depression & loss of reflexes (calcium gluconate is an appropriate treatment)
          • Halves the risk of eclampsia
  • Avoid diuretics & hyperosmolar agents, as well as limit IV fluids.
  • Early referral for delivery planning

Post-Partum Preeclampsia

Preeclampsia is generally cured by delivery of the placenta, however in some women the disease process can worsen during the first 48 hours following delivery. Delayed postpartum preeclampsia can be defined as signs and symptoms of the disease leading to readmission more than two days but less than six weeks after delivery. These presentations are usually atypical and these women might be at risk for pulmonary oedema, renal failure, HELLP syndrome, postpartum eclampsia and stroke and therefore warrant close observation & followup.

One particular study (retrospectively following 152 patients with delayed post-partum preeclampsia) demonstrated ~63% had no antecedent diagnosis of hypertensive disease. 14.5% went on to develop eclampsia. The most common presenting complaint was headache (69.1%)

For your general presentation of post-partum headache, I would strongly recommend this paper for a concise straightforward approach.

References. 

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