Differentiaaldiagnose bij patiënten bij wie een anoxisch-ischemisch coma wordt vermoed

\u3cp\u3eThree case studies illustrate that suspected anoxic-ischaemic coma often requires careful differential diagnosis to detect treatable conditions. A 47-year-old man underwent cardiopulmonary resuscitation for ventricular fibrillation caused by myocardial ischaemia. He exhibited rhythmic eyelid movements while in a coma. Epilepsy was suspected, and the patient regained consciousness after being treated with antiepileptic drugs. A 34-year-old man underwent cardiopulmonary resuscitation for multiple episodes of ventricular fibrillation. Treatment was directed toward myocardial ischaemia and included anticoagulants. The patient had bilateral, fixed dilated pupils. A CT of the brain showed traumatic contrecoup haemorrhage in the left temporal lobe with signs of transtentorial herniation. The patient died. A 74-year-old woman was found unconscious at home. An ECG performed by the paramedics showed ST segment elevation in the precordial leads. Anoxic-ischaemic coma following cardiac arrest was suspected. However, a coronary angiogram was normal and a CT of the brain revealed subarachnoid haemorrhage caused by a ruptured intracranial aneurysm. She recovered after cranial surgery.\u3c/p\u3

Myocarditis in patients with subarachnoid hemorrhage: A histopathologic study

Cardiac abnormalities after subarachnoid hemorrhage (SAH) such as electrocardiographic changes, echocardiographic wall motion abnormalities, and elevated troponin levels are independently associated with a poor prognosis. They are caused by catecholaminergic stress coinciding with influx of inflammatory cells into the heart. These abnormalities could be a sign of a myocarditis, potentially giving insight in pathophysiology and treatment options. These inflammatory cells are insufficiently characterized, and it is unknown whether myocarditis is associated with SAH. Myocardium of 25 patients who died of SAH and 18 controls was stained with antibodies identifying macrophages (CD68), lymphocytes (CD45), and neutrophil granulocytes (myeloperoxidase). Myocytolysis was visualized using complement staining (C3d). CD31 was used to identify putative thrombi. We used Mann-Whitney U testing for analysis. In the myocardium of SAH patients, the amount of myeloperoxidase-positive (P<.005), CD45-positive (P<.0005), and CD68-positive (P<.0005) cells was significantly higher compared to controls. Thrombi in intramyocardial arteries were found in 22 SAH patients and 1 control. Myocytolysis was found in 6 SAH patients but not in controls. Myocarditis, consisting of an influx of neutrophil granulocytes, lymphocytes, and macrophages, coinciding with myocytolysis and thrombi in intramyocardial arteries, occurs in patients with SAH but not in controls. These findings might explain the cardiac abnormalities after SAH and may have implications for treatment. (C) 2015 Elsevier Inc. All rights reserved