A comatose, circulatory stable, but hypoventilating patient was intubated at the scene and brought in to the emergency department by ambulance. The past medical history, which was provided by his grandmother, revealed that this 39-year-old man had lived with her for many years. The previous weeks prior to presentation he complained of fatigue and recurrent nose bleeds, and he was eating irregularly. At the age of 3 he had been operated on a benign cerebral gangliocytoma and had been on antiepileptic medication because of generalized seizures for some years. The patient had not seen a doctor for many years. Physical examination revealed a patient in a dishevelled condition with bilateral vesicular breathing and distant but regular heart sounds without any murmur, rare bowel sounds, no tenderness to deep palpation, and nonpitting oedema of the legs. His body temperature was slightly elevated (38.5 C). The neurologic examination showed equal pupils reactive to light symmetric muscle tone and absence of plantar reflexes.
On admission, laboratory data showed significantly decreased levels of sodium and potassium (sodium: 120 mmol/L, potassium: 2.9 mmol/L) as well as increased levels of creatine kinase (overall-CK: 967 U/L, CK MB 6.7 microg/L (norm CK MB < 7.7 g/L in males)) and glutamate- oxalacetate-transaminase (AST: 62 U/L). The coagulation panel demonstrated a slightly increased international normalised ratio (INR: 1.4) and partial prothrombin time (PTT: 37 s). The complete blood count showed a normochromic normocytic anaemia (haemoglobin: 114 g/L), with normal platelets and leucocytes. The arterial blood gas on admission showed an alkalosis (pH 7.43) with an increased bicarbonate of 31.8 mmol/L (base excess of +7), but as well increased pCO2 of 6.4 kPa. The remaining results were unremarkable including normal liver function tests, glucose levels, and creatinine and urea. A urinary toxicological screening showed no signs of intoxication with benzodiazepines, opiates, amphetamines, tricyclic antidepressants, acetaminophen, or salicylate.
The electrocardiogram (ECG) showed a sinus rhythm (85 bpm), normal axis, and an incomplete right bundle branch block (RBBB). The QTc time was within normal range. A computer tomography with angiography of the cerebral arteries (Angio-CT) showed a frontobasal intracerebral bleeding with irruption into the ventricles. A cerebral aneurysm and skull fracture were excluded (Figure 1). A chest X-ray (CXR) showed impressive cardiomegaly without any signs of chest infection or congestive heart failure (Figure 2). An echocardiogram showed a large pericardial effusion with swinging heart but without compromise of right ventricular function and a normal variation of mitral inflow (Figure 3). Significant valve dysfunction was excluded and normal systolic and diastolic left ventricular function and size of heart chambers confirmed. The patient was transferred to the intensive care unit (ICU). Analgosedation with propofol and fentanyl and Continuous Positive Airway Pressure (CPAP) ventilation was continued (positive end expiratory pressure (PEEP): 5 and pressure support (ASB): 5-10 mmHg, inspiratory oxygen concentration FiO2: 40%). To maintain a MEAN blood pressure of 65 mmHg low-dose support with noradrenaline was needed. A supplementation of potassium and sodium was performed. An electric encephalogram (EEG) showed a left frontopolar epileptic focus, so that therapy with levetiracetam was started. Further, diagnostic needle pericardiocentesis was performed and 1300 mL of slightly haemorrhagic pericardial fluid evacuated (glucose 11.5 mmol/L, protein 73 g/L, albumin 44 g/L, lactate dehydrogenase (LDH) 173 U/L, red blood cells: few, and white blood cells 0,21 x 109 (25% neutrophils, 2% lymphocytes)), Gram stain and bacterial cultures were negative, cytology was negative for malignant cells, and polymerase chain reaction (PCR) for tuberculosis was negative.
About four hours after this procedure the patient went into cardiac arrest (pulseless electrical activity, PEA) caused by cardiac tamponade. Though the pericardial tube was still in place it was obstructed by coagulated blood. A second needle pericardiocentesis was performed and a significant amount of deeply red haemorrhagic cardiac effusion could be removed, which resolved the patient's deterioration immediately. Further work-up of the hyponatremia (120 mmol/L) could exclude pseudohyponatremia (serum osmolality: 267 (normal range: 280-300 mmol/kg)) and adrenal insufficiency by an adrenocorticotropin hormone (ACTH) stimulation test (cortisol basal: 919 nmol/L, 30 min after stimulation with 250 mug ACTH: 1137 nmol/L, and 60 min: 1235 nml/L). Urine osmolality was 610 mmol/kg and urine sodium content was 39 mmol/kg. Additionally, the thyrotropin level was significantly increased at 112 (normal range 0.33-4.49 mlU/L) accompanying T4 and T3 levels of 1.2 (normal range: 66-181 pmol/L) and 0.4 (normal range: 1.1-3.2 pmol/L), respectively. Thyroid peroxidase (TPO) antibodies could be shown to be significantly increased to 294 IU/mL (normal range: 100-200 U/L). As Hashimoto thyroiditis was found as underlying pathomechanism, the patient was treated with 100 mug levothyroxine once daily and the patient could be extubated five days after admission. Fortunately he was only slightly neurologically impaired (GCS 14, with no signs of cerebral nerve paralysis but decreased muscular strength in all four extremities (M3/4)). Due to recurrence of the pericardial effusion in echocardiographic follow-up, a thoracoscopic pericardial fenestration was performed about 3 months after the ICU stay.