Intracranial Complications of Cocaine Abuse

Emerg Med 40(10):37, 2008

By Carlos J. Roldan, MD, FAAEM, FACEP, and Meeta M. Patel, DO

Regular intranasal cocaine abuse can create a breeding ground for infection that can lead to chronic sinusitis and other serious complications. The authors present a case in point.

A young man is brought to the emergency department by his college roommate. “He hasn’t left his bedroom in three days,” the roommate reports. The patient has had sinusitis, with a persistent frontal headache and little appetite, for the past three weeks. The sinusitis, which is worsening, has been treated with levofloxacin and antihistamines, which had improved his symptoms somewhat. However, he has since become increasingly lethargic, and three days earlier he woke up with a “swollen forehead.”

The patient has no history of prior sinusitis, trauma, or any other medical problems. He has no past surgeries, allergies, or family history of sinusitis or allergies, but admits to snorting cocaine socially, at parties and on weekends.

Although the patient is pale and emaciated, his vital signs are normal: heart rate, 88; blood pressure, 128/74; temperature, 98.7°F; respirations, 20. He has a Glasgow Coma Scale score of 15.

Physical examination finds a right frontal mass (5 cm by 4 cm in size) on his forehead, which seems tender to palpation. The mass appears to be connected to the cranial and facial skeletal structures and has surrounding soft tissue swelling, but without involvement of the orbits or nasal cavity. The examining physician feels no fluctuation, warmth, or erythema.

The rest of the examination reveals dry oral mucosa, a supple neck without palpable masses, and lungs clear on auscultation. Heart sounds are normal, with no obvious murmurs. The abdomen is flat and soft, without masses or organomegaly. The neurologic exam is normal; no meningeal signs are present. 

Initial treatment consists of a normal saline bolus and intravenous morphine for pain control. Basic laboratory tests (including chemistry, urinalysis, urine drug screen, total creatine phosphokinase, and blood cell counts) reveal a total white blood cell (WBC) count of 12,600 with 86% neutrophils and no bands. No other abnormalities are reported, except for confirmatory cocaine metabolites in the urine.

A computed tomography (CT) scan of the head without contrast shows a right frontal lobe mass consistent with an intraparenchymal abscess, osteomyelitis of the frontal bone, extensive sinusitis, and a right scalp mass compatible with a Pott puffy tumor (see images below). Following this, blood cultures and lactate levels are added to the orders. The patient is started on intravenous ceftriaxone and vancomycin.

Noncontrast CT scan of the head and brain (blood/brain window). A right frontal lobe intraparenchymal hypodense lesion compatible with a cerebral abscess is shown. A surrounding shadow composed of mixed densities is consistent with inflammatory tissue (bottom arrow). There is also evidence of severe frontal scalp edema with mixed densities consistent with a scalp abscess or a Pott puffy tumor (top arrow). Noncontrast CT scan of the head and brain (bone window). Generalized thickening of the sinus mucosa is apparent. This noncontrast CT scan also shows evidence of irregular density of the maxillary bone consistent with osteomyelitis and extensive sinusitis (arrow).

Neurosurgery is consulted and the patient is admitted for further treatment. The antibiotics are continued. He undergoes therapeutic craniotomy on day 3, and pathology of the debrided cerebral and bone specimens is consistent with brain abscess and surrounding osteomyelitis. An initial Gram stain shows many WBCs but no organisms. Final cultures, however, are all negative and lactate levels are normal.

Magnetic resonance imaging of the head and brain (enhanced view). A right frontal lobe abscess with surrounding edema (top arrow) and frontal extracranial soft tissue edema compatible with scalp abscess (bottom arrow) are evident.   Magnetic resonance imaging of the head and brain with intravenous contrast. This image shows a detailing of the extension of a large right frontal lobe brain and a frontal scalp subcutaneous abscess (Pott puffy tumor), connected by a full-thickness erosion of the frontal bone consistent with chronic osteomyelitis (arrow).

The patient progresses well, but magnetic resonance imaging (MRI) two weeks later (with and without contrast) finds a residual right frontal abscess (see images above). He is taken to the operating room again for evacuation of the abscess. He experiences no complications and is discharged from the hospital on day 28 without neurologic sequelae.

ENVIRONMENT FOR INFECTION

Cocaine produces its euphoric effects by acting as a potent neuroendocrine stimulator that blocks the release and reuptake of catecholamines and, with less intensity, of serotonin and dopamine, particularly in the limbic system and ventral basal nuclei. Locally, cocaine has an anesthetic effect via sodium and potassium channel blockade, which reduces the resting membrane potential, thus prolonging duration of the action potential. The direct vasoconstrictive effect of cocaine is responsible for some of the drug’s unique anesthetic properties as well as some of the complications associated with its recreational use. Infections,  for instance, are common. The intense vasoconstriction reduces oxygen tension, which facilitates local necrosis, followed in many cases by a bacterial overgrowth (most commonly of anaerobic pathogens).

A Pott puffy tumor is a subperiosteal abscess secondary to osteomyelitis adjacent to an intracranial infection, usually chronic sinusitis. This rare condition was first described in 1760 by Sir Percivall Pott as a “puffy, circumscribed, indolent tumor of the scalp” resulting from trauma to the frontal bone. The mucosal hyperemia and plugged sinus ostia usually found in chronic sinusitis cause a decrease in oxygenation within the sinus, delineating the common pathway that evolves into an indolent frontal edema with or without the systemic manifestations representative of a Pott puffy tumor.

Chronic use of cocaine has been associated with midfacial osteomyelitis, septal perforation, palatal necrosis, osteolytic sinusitis, and cribriform plate necrosis. There is not a clear direct link between the use of snorted cocaine and the presence of a Pott puffy tumor. However, multiple reports have established that snorting cocaine predisposes to chronic sinusitis and that chronic sinusitis can lead to the development of a Pott tumor.

Cerebral abscess is an uncommon but serious condition that can affect patients of any age. It is a very rare complication of sinusitis, especially in the young, immune-competent patient. The majority of brain abscesses originate from the direct invasion of pathogens from the sinuses, middle ear, or oral cavity after colonization of the oropharynx. The most common etiologic agents are the Streptococcus milleri group, including S. anginosus, S. constellatus, and S. intermedius, but anaerobic streptococci, Haemophilus, Bacteroides, and Fusobacterium are also frequently isolated in brain abscesses.

Other mechanisms of abscess formation emerge from the seeding of organisms from distant infections through the blood-brain barrier. About 20% to 30% of cases are considered idiopathic.

URINARY TRACT INFECTION: MOST COMMON CAUSE

Urinary tract infection (UTI) is the most common cause of dysuria, accounting for 11 million office visits, 1.7 million emergency department visits, and 100,000 hospitalizations annually, with a health care cost of nearly $2.5 billion. Neonates, girls, young women, and older men are most susceptible to UTIs. In women, bacterial cystitis is the most common bacterial infection. Every woman has a 60% lifetime risk of developing bacterial cystitis; one-third of all U.S. women develop the infection before the age of 24. By contrast, men have a lifetime risk of only 13%.

Urinary tract infection is defined as significant bacteriuria with such signs and symptoms as dysuria, hematuria, increased urinary frequency, urgency, hesitancy, suprapubic discomfort (present in only 15% to 20%), and costovertebral angle tenderness. Infections may be acute or chronic.

Urinary tract infection is caused by pathogenic invasion of the urinary tract, which leads to an inflammatory response of the urothelium. Bacteria gain access to the urethral meatus by local contamination or sexual intercourse and ascend into the upper urinary tract. Escherichia coli causes the majority of UTIs (85% of community- and 50% of hospital-acquired UTIs). Staphylococcus saprophyticus causes 10% to 15%; Proteus mirabilis, Staphyloccus aureus, Enterococcus species, and Klebsiella species are responsible for the rest.

Nosocomial infections and those associated with foreign bodies may involve more aggressive organisms such as Pseudomonas aeruginosa, Serratia, Enterobacter, and Citrobacter species. Nonbacterial infections are uncommon but may be found in the immunosuppressed or patients with diabetes, with Candida species being the most common.

Patients at increased risk for UTI include those with obstructions or alterations in flow from tumors, stones and congenital anomalies, and disruption of the mucin layer from instrumentation. For men, bladder outlet obstruction secondary to BPH is another risk factor.

Women are at greater risk for UTI than men, partly because of the relatively short, straight anatomy of the urethra. Ascent of bacteria from the perineum is the most common cause of acute cystitis in women. Pregnancy and alterations in normal vaginal Lactobacillus colonization due to spermicides, antibiotics, and low levels of estrogen are additional risk factors for women. Sexually active women have a higher risk than women who are not sexually active.

SYMPTOMS TO WATCH FOR

The most common symptom associated with intracranial complications of a sinus, ear, or oral infection is an acute and progressive headache, as in the case of the patient presented here. Brain abscesses can also present with vomiting, with or without fever, and at other times with specific focal neurologic deficits. A history of sinusitis, gingivitis, dental caries, or otitis in the presence of these signs and symptoms should always lead the clinician to consider this diagnosis.

The abscess location may affect the clinical presentation. The direct spread of a frontal lobe abscess, for example, can manifest with vision loss due to orbital compromise or diplopia from reduced ocular movement. Proptosis, chemosis, and loss of the corneal reflex may also be seen if cranial nerves are involved as a result of cavernous sinus thrombosis.

A CT scan of the brain is the first choice for neuroimaging due to its availability, speed, and ability to visualize the sinus cavities and brain anatomy; both coronal and axial cuts are necessary to evaluate the extent of the infection. A CT scan of the brain with intravenous contrast or preferably MRI should be obtained if further information is needed or suspicion is high after a negative CT scan without contrast.

Treatment of brain abscesses begins with antibiotic coverage started in the emergency department. Abscesses of sinogenic origin are best treated with broad-spectrum antibiotics covering the S. milleri group, other aerobic organisms such as Haemophilus, and anaerobes including Bacteroides and Fusobacterium species. A third-generation cephalosporin combined with metronidazole is considered appropriate coverage. Blood cultures should be obtained prior to antibiotic administration so that the treatment can be better targeted.

Early consultation with neurosurgery and otolaryngology is recommended since intervention by both specialties may take place during surgery. Thanks to neuroimaging and better antibiotic regimens, mortality and morbidity due to brain abscess have declined dramatically and are currently estimated to be about 5% to 10%, although long-term sequelae such as seizure disorders, cognitive defects, hemiparesis, and other neurologic deficits are possible. Once almost always fatal, brain abscess now is less likely to kill if it’s treated early and aggressively.

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Suggested Reading Bair-Merritt MH, et al.: Suppurative intracranial complications of sinusitis in previously healthy children. Pediatr Infect Dis J 24(4): 384, 2005. Clark JR, et al.: Pott’s puffy tumor: a clinical variant. Aust N Z J Surg 69(10): 759, 1999. Kung SW, et al,: Poon WS. Pott’s Puffy Tumour. Hong Kong Med J 2002; 8(5):381, 2002. Lang EE, et al.: Intracranial compilations of acute frontal sinusitis. Clin Otolaryngol Allied Sci 26(6): 52, 2001. Mathisen G and Johnson P: Brain abscesses. Clin Infect Dis 25(4): 763, 1997. Noskin GA and Kalish SB: Pott’s puffy tumor: a complication of intranasal cocaine abuse. Rev Infect Dis 13(4): 606, 1991. Nunez DA: Presentation of rhinosinogenic intracranial abscesses. Rhinology 29(2); 99, 1991. Osborn MK and Steinberg JP: Subdural empyema and other suppurative complications of paranasal sinusitis. Lancet Infect Dis 7(1): 62, 2007. Panacek EA: Cocaine. In Hall JB, et al. (eds) Principles of Critical Care, McGraw-Hill, 1992, p. 2148. Talbott JF, et.: Midfacial osteomyelitis in a chronic cocaine abuser: a case report. Ear Nose Throat J 80(10): 738, 2001. Younis RT, et al.: The role of computed tomography and magnetic resonance imaging in patients with sinusitis with complications. Laryngoscope 112(2): 224, 2002.

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