Introduction

Pituitary apoplexy is a neurosurgical emergency in which prompt intervention may halt and even reverse associated neurologic deficits and possible mortality. The condition results from hemorrhage or necrosis of a pituitary tumor. It has been found to occur in 0.6 to 10.5% of all pituitary adenomas. ¹

In 1950, Brougham was the first to describe the clinical and pathologic findings of five patients who presented with changes in mental status, headaches, meningismus, and ocular disturbances. ² Since then, there has been extensive interest in the entity as well as considerable debate on what the term pituitary apoplexy encompasses. In fact, there have been reports of silent pituitary apoplexy. ³ Mohr estimated the incidence of asymptomatic hemorrhages in pituitary adenomas to be 9.9% as opposed to 0.6% that presented with clinical findings. ⁴ Furthermore, Onesti described five patients with subclinical pituitary apoplexy, that is, a clinically silent yet extensive hemorrhage into a pituitary adenoma. ⁵

With such a broad interpretation in the literature it is increasingly helpful to define the diagnosis of pituitary apoplexy by clinical parameters that include the sudden onset of headache, meningismus, visual impairment, and occulomotor abnormalities in varying combinations along with radiologic evidence of hemorrhage in or sudden expansion of a pituitary adenoma.

Indications

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  Diagnosis of apoplexy requires evidence of hemorrhage or rapid expansion on either computed tomography (CT) or magnetic resonance imaging (MRI) within a preexisting adenoma as well as clinical correlation.

  
  
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  Patients often present with sudden onset of headache, meningismus, disturbances of mental status, and ocular findings that can range from ophthalmoplegia and visual field defects to monocular or binocular blindness.

  
  
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  Bacterial and viral meningitis, intracerebral hematoma, optic neuritis, brainstem infarction, temporal arteritis, encephalitis, transtentorial herniation, cavernous sinus thrombosis, and migraine may all in one form or another mimic an acute pituitary vascular accident. ^{1 , 6}

  
  
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  The most important entity that must be considered and excluded is an aneurysmal subarachnoid hemorrhage. ^{7 , 8}

  
  
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  A ruptured Rathke’s cleft cyst, though rare, may also mimic pituitary apoplexy. ^{9 , 10}

  
  
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  Initial medical stabilization with intravenous fluid and steroids is required in all cases to correct the profound hypoadrenalism that may result.

  
  
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  Transsphenoidal resection is considered for those with continued neurologic deficit after initial conservative therapy, and immediately for those with loss of acuity and/or fields. ⁶

  
  
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  While ophthalmoplegia has been shown to correct as frequently with conservative management as with surgical intervention, ^{11 – 13} surgical resection offers the most hope of improving visual field and acuity deficits. Many studies have suggested that decompression within 1 week may offer the best chance of visual recovery. ^{11 , 14} Others have shown improvement with decompression months after initial visual loss. ¹⁵

Preprocedure Considerations

Radiographic Imaging

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  CT without contrast is most valuable the first 2 days of hemorrhage ( Fig. 22.1 ).

  
  
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  After 48 hours, MRI is more sensitive, as it can better delineate older blood from tumor and areas of necrosis from cystic changes ( Fig. 22.2 ). The MRI is also helpful in estimating the age and time course of the hemorrhage. Hemorrhages less than 7 days will appear hypo- to isointense on T1- and T2-weighted images. During the second week a hyperintense signal can be found bordering the hematoma. By the second week increasing hyperintensity will be seen throughout the hematoma on both T1- and T2-weighted images.

  
  
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  If clinically warranted, an angiogram or magnetic resonance angiogram (MRA) should be obtained if neither CT nor MRI is able to rule out a concomitant aneurysm.

  
  
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  MRI will also best demonstrate the extension of the tumor or hemorrhage into the suprasellar space as well as chiasmal compression and cavernous sinus extension. Furthermore, the intracarotid distance can be delineated in order to avoid injury during surgical resection.

Related posts:

19 Removal of Spontaneous Intracerebral Hemorrhages 21 Ventricular Shunt Malfunction 20 Surgery for Acute Intracranial Infection 7 Invasive Neuromonitoring Techniques 18 Treatment of Acute Cauda Equina Syndrome 23 Combat Cranial Operations

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