Headaches of increasing intensity for a week after using crack cocaine.
Article Type: Case study
Subject: Crack (Drug) (Health aspects)
Hematoma (Risk factors)
Hematoma (Diagnosis)
Hematoma (Care and treatment)
Hematoma (Case studies)
Hypertension (Risk factors)
Hypertension (Diagnosis)
Hypertension (Care and treatment)
Hypertension (Case studies)
Authors: Glancy, Luke
Nijjar, Vikram S.
Pub Date: 01/01/2011
Publication: Name: Baylor University Medical Center Proceedings Publisher: The Baylor University Medical Center Audience: Academic Format: Magazine/Journal Subject: Health Copyright: COPYRIGHT 2011 The Baylor University Medical Center ISSN: 0899-8280
Issue: Date: Jan, 2011 Source Volume: 24 Source Issue: 1
Geographic: Geographic Scope: United States Geographic Code: 1USA United States
Accession Number: 245483190

A 49-year-old man complained of worsening headaches after using crack cocaine a week earlier. He had a slow heart rate (32 beats per minute) and high blood pressure (174/90 mm Hg), and an electrocardiogram recorded on admission showed sinus bradycardia with junctional escape complexes (Figure).

The patient was confused but responsive; his Glasgow coma scale was E3, V4, M6, for a total of 13. A computed tomogram of the head without contrast material showed a left frontoparietotemporal subdural fluid collection 2.3 cm thick and a 1.5 cm left-to-right midline shift. A subacute subdural hematoma was evacuated through burr holes, and the patient was able to leave the hospital.

As recognized by Cushing over a century ago, a slow heart rate and high blood pressure can be signs of increased intracranial pressure, which in its most severe form may be accompanied by a slow respiratory rate and followed by death (1, 2). Subsequent experimental studies have shown that the triad of high blood pressure, slow heart rate, and slow respirations described by Cushing, and also known as Cushing's reflex, response, or phenomenon, often begins with hypertension and tachycardia, with the tachycardia being replaced by bradycardia by the time the patient presents (3-5). The pathophysiological cascade begins with an increase in intracranial pressure that diminishes brain-stem perfusion. This in turn activates the sympathetic nervous system, resulting in elevated blood pressure and tachycardia. The systemic hypertension acts on the carotid baroreceptors and the heart rate reflexly slows, resulting in bradycardia with high blood pressure, which may be acute, subacute, as in this patient, or even chronic depending on the timing of the onset and relief of the increased intracranial pressure (3-5).

(1.) Cushing H. Concerning a definite regulatory mechanism of the vasomotor centre which controls blood pressure during cerebral compression. Bull Johns Hopkins Hosp 1901;12:290-292.

(2.) Cushing H. The blood pressure reaction of acute cerebral compression, illustrated by cases of intracranial hemorrhage. Am J Med Sci 1903;125:1017-1044.

(3.) Heymans C. The control of heart rate consequent to changes in the cephalic blood pressure and in the intracranial pressure. Am J Physiol 1928;85:498-505.

(4.) Kalmar AF, Van Aken J, Caemaert J, Mortier EP, Struys MM. Value of Cushing reflex as warning sign for brain ischaemia during neuroendoscopy. Br J Anaesth 2005;94(6):791-799.

(5.) Wan WH, Ang BT, Wang E. The Cushing response: a case for a review of its role as a physiological reflex. J Clin Neurosci 2008;15(3): 223-228.

D. Luke Glancy, MD, and Vikram S. Nijjar, MD

From the Sections of Cardiology, Departments of Medicine, Louisiana State University Health Sciences Center and the Medical Center of Louisiana, New Orleans.

Corresponding author: D. Luke Glancy, MD, 7300 Lakeshore Drive, #30, New Orleans, Louisiana 70124 (e-mail: dglanc@lsuhsc.edu).
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