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Published 22 July 2009, doi:10.1136/bmj.b2864
Cite this as: BMJ 2009;339:b2864
Marieke van Onna, resident in internal medicine, Thomas van Bemmel, internist, Erik van Wensen, neurologist, Cees Schaar, internist-haematologist, Hein Slis, radiologist, Peter E Spronk, internist-intensivist
1 Department of Intensive Care Medicine, Gelre Hospitals, 7334 DZ Apeldoorn, Netherlands
Correspondence to: P E Spronk p.spronk{at}gelre.nl
A comatose 29 year old male was brought to the emergency department of our hospital. The patient was an international truck driver, and he and his co-driver had slept the night before in their truck at a car park near the motorway. The next morning, the co-driver found the patient in a comatose state in the sleep cabin of their truck. The attending neurologist observed a Glasgow coma score of four (E1-M2-V1) with fixed dilated pupils and no cornea and ocular cephalic brainstem reflexes. Furthermore, the patient had multiple petechiae on the left side of the throat and symmetrical bruises on the anterior medial side of both upper legs. Otherwise, physical investigation was unremarkable.
Short answers
Long answers
1 Investigations
The initial investigations conducted on a patient who is comatose without apparent cause should aim to identify treatable causes like infections, metabolic derangements, and intoxications. The panel of laboratory tests undertaken should at the very least include a complete blood count; blood testing for electrolytes; renal and liver function tests; blood glucose test; and arterial blood gas analysis. Prothrombin and partial thromboplastin time should be added whenever lumbar puncture is considered or general examination suggests a clotting disorder.
Computed tomography is the diagnostic modality of choice to screen for intracerebral pathology. A lumbar puncture should be performed to rule out meningitis in patients who have fever or hypothermia. If these tests do not identify the underlying cause, further appropriate tests include electrocardiography, blood cultures, thyroid function tests, electroencephalography, and brain magnetic resonance imaging.1 2 3 Comprehensive drug testing has little impact on the management of comatose patients.4
2 Diagnosis
Most comatose patients who present at the emergency department have experienced trauma or have cerebrovascular disease, are intoxicated, or have metabolic derangements. Careful general and neurological examination of the patient might provide valuable clues to the underlying cause of the coma; in particular a survey of the skin and mucosa can be very illuminating.
Our patient presented with petechiae and bruises. Petechiae (and ecchymoses) can be seen with some infections (for example, meningococcal sepsis and Rocky Mountain spotted fever) and with some types of bleeding diathesis (such as disseminated intravascular coagulation and thrombocytopaenia). Petechiae confined to the head and neck might be caused by acutely raised venous pressure—for example, from strangulation of the neck—or by convulsive seizures. Bruises usually indicate trauma, with "raccoon eye" (periorbital ecchymosis) and Battles sign (bruising over mastoid) suggesting traumatic brain injury.1
On the basis of the general examination findings (absence of either hyperthermia or hypothermia, normal vital signs and breathing pattern, and the distribution of the petechiae and bruises) and the absence of focal neurological deficits, physical abuse was the most likely diagnosis for this patient. In males between 25 and 35 years, intracranial damage is about seven times more likely to be caused by non-natural causes (including physical abuse) than by cerebral vascular accidents.5 It is, therefore, necessary that health care personnel have a high index of suspicion of the possibility of physical abuse in comatose patients, especially in young males.
Patient outcome
Computed tomography revealed a large intraparenchymatous cerebral haematoma in our patient, with breakthrough to the ventricular system and complete compression of the right ventricular system. Remarkably, there was no visible fracture of the skull. Imaging of the thorax and abdomen revealed an enlarged spleen and multiple small lymph nodes.
Laboratory results showed a haemoglobin level of 7.1 g/l, a white blood cell count of 227x109/l, a platelet count of 35x109/l, an activated partial thromboplastin time of 50 sec, and a prothrombin time of 32.2 sec. A peripheral blood smear showed 80% myeloblasts with Auer rods. Hence, the patient was diagnosed with acute myeloid leukaemia. Given the fatal prognosis of cerebral haematoma in combination with apparent acute myeloid leukaemia, medical treatment was judged to be futile and was stopped.
Conclusion
This case illustrates that every patient needs to be examined thoroughly. Moreover, every physician needs to judge clinical symptoms with an open mind and a proper differential diagnosis. The clue in our patient was the apparent discrepancy between the severe intracerebral bleeding and the absence of a skull fracture. The diagnosis was straightforward thanks to further investigative tests; if the patient had died before arrival to the emergency department, however, the coroner might have judged differently.
Cite this as: BMJ 2009;339:b2864
Patient consent not required (patient anonymised, dead, or hypothetical).
Provenance and peer review: Commissioned; externally peer reviewed.