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Cocaine abuse and unusual injection sites
CORRESPONDENCE
Ibuprofen Blood Levels Vary To the Editor: We welcomed the Hall et al article, "Ibuprofen Overdose: 126 Cases" [November 1986; 15:1308-1313] in its presentation of their nomogram and concise discussion of ibuprofen overdose symptomatology. We would like to add a sampling of four patients ingesting ibuprofen (and in w h o m levels were obtained) presenting to our emergency department within the previous six months. Case I. An 18-year-old, 70-kg w o m a n presented four hours after ingestion of 50 600-mg ibuprofen tablets {428 mg/kg). She was alert and asymptomatic. Her physical examination was unremarkable except for superficial lacerations over the volar aspects of her wrists. The patient's vital signs were blood pressure, 130/90 m m Hg; pulse, 76; respirations, 20; and afebrile. Treatment consisted of ipecac, activated charcoal with sorbitol, and tetanus-diphtheria toxoid. Toxicology screen five hours after ingestion demonstrated only ibuprofen at 38 ~g/mL. Serum electrolytes, BUN, and creatinine were all within normal limits. The patient remained asymptomatic and was transferred for psychiatric evaluation after six hours observation in the ED. Case 2. An 18-year-old, 75-kg man was transported to the ED after ingestion of 80 600-mg ibuprofen tablets (640 rag/ kg). The patient was obtunded, and responded only to noxious stimuli with combative behavior, without verbalization. Physical examination was otherwise remarkable only for nonreactive, 1-mm pupils. Vital signs were blood pressure, 120/60 m m Hg; pulse, 130; and respirations, 20. No response was noted with naloxone or DS0 W. The patient was intubated and paralyzed with vecuronium prior to gastric lavage and gastric installation of activated charcoal and sorbitol. Toxicology screen two hours after ingestion demonstrated ibuprofen level of 520 ~g/mL; ethanol, 106 mg%; and salicylates, 3.5 mg%. He remained intubated for 12 hours, and intermittent episodes of hypotension (systolic blood pressure, 80 to 100 mg Hg) were treated with isotonic fluid boluses. Subsequent ibuprofen levels at 4, 6.5, and 11.5 hours after ingestion were 320 p,g/mL, 124 ~g/mL, and 9.5 p,g/mL, respectively. Of note, this patient developed a severe hypophosphatemia (PO4, 0.8 mg/dL), as well as a hypokalemia {requiring 160 mEq KC1 IV over the first 12 hours to maintain K + at 3.6 mEq/L) following his ingestion. He was discharged six days after admission after noting a mild rise in AST (33 to 61 IU/L), ALT (30 to 80 IU/L) and LDH {207 to 386 IU/L), which subsequently resolved. Renal failure never developed. He developed chicken pox two days after admission.
Case 3. A 16-year-old, 55-kg girl presented two hours after ingestion of 28 600-mg ibuprofen tablets (305 mg/kg). She was alert with complaints of headache and tinnitus. Physical examination was unremarkable. Vital signs were blood pressure, 150/82 m m Hg; pulse, 118; respirations, 16; and afebrile. Treatment consisted of naloxone, ipecac, and activated charcoal with sorbitol. Toxicology screen at four hours after ingestion reported only ibuprofen at 37 ~g/mL. Serum electrolytes, BUN, and creatinine were all normal. The patient remained asymptomatic and was discharged after six hours of observation in the ED. Case 4. A 21-year-old woman presented one hour after ingestion of 20 800-mg ibuprofen tablets (200 mg/kg). She was alert and asymptomatic, with an unremarkable physical examination. Vital signs were blood pressure, 142/74 m m Hg; pulse, 92; respirations, 20; and afebrile. Treatment consisted of ipecac and activated charcoal with sorbitol. Toxicology screen two hours after ingestion demonstrated only trace ibuprofen in the blood. She remained asymptomatic, and was transferred for psychiatric evaluation after six hours of observation in the ED. These four cases demonstrate the variability of measured ibuprofen blood levels, reported a m o u n t s ingested, and syrnptomatology in adults; as such, they correlate well with the findings of Hall et al. Of interest is our second case, in which the patient developed a marked potassium and phosphate deficit following ingestion. There is no reason to suspect that this was due to either the other drugs he ingested or was iatrogenic in nature. These abnormalities have not been described previously in ibuprofen ingestions. Though the rise in AST, ALT, and LDH was minor, it is difficult to determine if this was sec o ondary to his ingestion or his exposure to varicella. These evaluations are not clinically signifieant and have been noted previously1, ~ in those taking normal quantities of ibuprofen, but not in single-dose ingestions. Fred Harchelroad Jr, MD Timothy C Evans, MD Elgin Hobbs, MD Division of Emergency Medicine Allegheny General Hospital Pittsburgh, Pennsylvania 1. Stempel DA, Miller JJ: Lymphopenia and hepatic toxicity with ibuprofen, l Pediatr 1977;90:657-658. 2. Royer GL, Seckman CE, Welshman IR: Safetyprofile: Fifteen years of clinical experiencewith ibuprofen. Am l Med 1984~77:25-34.
Cocaine Abuse and Unusual Injection Sites To the Editor: As the illicit use of cocaine has continued to increase, so too have cocaine-related emergency department visits, hospital admissions, and deaths.~ Cocaine is most often taken 118/186
mtranasally.Z It also may be injected subcutaneously, IM or IV; taken orally, vaginally, sublingually, or rectally; and may be smoked, a For the IV drug abuser, potential routes of ad-
Annals of Emergency Medicine
17:2 February 1988
ministration become harder to identify as superficial veins thrombose and sclerose. The use of the breast, a highly vascular and accessible organ, as the point of entry for drug injections is not well recognized by physicians. 4 We report a case of injection of cocaine into a superficial vein of the breast with resultant breast infection, septic shock, and death. A 45-year-old woman was seen in the ED of DC General Hospital one week after injecting cocaine into a superficial vein of the upper right breast. Five days earlier she had been evaluated in a walk-in clinic with a temperature of 38.9 C orally and vague somatic complaints. No breast abnormality was recognized and she was sent home. On physical examination the patient was afebrile. Vital signs were blood pressure, 72/40 m m Hg; respirations, 40; and pulse, 130. The patient was obese with large breasts. The right breast had a 10 cm x 6 cm dark superficial ulceration in the upper outer quadrant with a surrounding zone of erythema. The involved breast was not crepitant. Old needle tracts were seen over the legs, arms, and hands. Laboratory studies included a white blood cell count of 3,500/nlrn3; arterial blood gases on room air were pH, 7.33; PCO2, 26; and PO2, 57. Chest roentgenogram showed interstitial edema consistent with early adult respiratory distress syndrome. ECG revealed a sinus tachycardia. The patient was admitted to the M I C U w i t h a presumptive diagnosis of septic shock secondary to a breast infection. Increasing respiratory distress prompted endotracheal intubation and mechanical ventilatory support. D o p a m i n e started at 2.5 ~xg/kg/min was increased progressively to maintain a systolic blood pressure of 90 m m Hg. Fine-needle aspiration of the right breast did not demonstrate any significant fluid collection. G r a m stain of scant right breast aspirate revealed Gram-positive cocci. After blood, urine, and sputum cultures were obtained, IV antibiotics were started empirically (vancomycin hydrochloride 500 m g every six hours; clindamycin phosphate 600 mg every six hours; and a single dose of gentamicin 150 rag) and a surgical consultation was called. Before surgical intervention could be instituted the patient became bradycardic and suffered a cardiopulmonary arrest from which she could not be resuscitated. Approximately 12 hours after presentation to the ED she was pronounced dead. At autopsy, there was diffuse suppurative inflammation of the right breast, including the overlying s u b c u t a n e o u s tissue and underlying muscles of the right upper chest wall. This process extended just beyond the midline to the left. Microscopic sections of the breast confirmed an extensive suppurative inflammatory process. Abscess formation in the nonlactating breast is uncommon.S Etiologic factors include major duct disease, concomitant cutaneous infection elsewhere, and chronic illness known to predispose to infection (eg, diabetes mellitus). The most c o m m o n organism isolated from abscesses in the nonlactating breast is staphylococcus. 6 Breast abscesses caused by injection of illicit drugs should respond to treatment m u c h as localized suppuration elsewhere in the body. Incision and drainage or excision should result in satisfactory and lasting resolution of the inflam17:2 February 1988
matory process in a majority of cases. Antibiotic therapy is an important adjunct to the surgical procedure. Because staphylococci are the most c o m m o n infecting organisms, the empiric use of a penicillinase-resistant penicillin is advised.7 Soft tissue infections in illicit drug abusers are often polymicrobial. Webb and T h a d e p a l l i reported r e c o v e r y of anerobes in 14 of 21 patients (67%) with severe soft tissue infections, and advised initial therapy with clindamycin and an aminoglycoside.90rangio et al commonly recovered anerobes, enteric Gram-negative aerobes, and oropharyngeal organisms from a similar group of patients. They recommended a semisynthetic penicillin with an antistaphlococcal activity, such as nafcillin or oxacillin, combined with an aminoglycoside to cover the high incidence of Gram-negative enteric anerobes. 9 In our case, the site of injection of cocaine was unusual and the potential for life-threatening infection unrecognized. The local necrotizing effect of the drug was analogous to the effect of cocaine on the nasal septum in intranasal abusers and undoubtedly contributed to the extensive inflammatory process found within the breast.lo Although fine-needle aspiration did not suggest an undrained collection, the clinical setting and physical findings we described should prompt an early and aggressive incision and drainage procedure. Physicians need to be aware of the enormity of the threat that cocaine abuse represents in this country. Moreover, they need to recognize the stigmata of cocaine abuse, including injection of this drug into unusual sites such as the breast. R i c h a r d W Holt, M D D a n i e l L Miller, M D G e o r g e t o w n U n i v e r s i t y Surgical D i v i s i o n DC General Hospital Washington, DC
1. Gay ~R: Clinical management of acute and chronic cocaine poisoning.
Ann Emerg Med 1982;11:562-572.
2. Washton AM, Gold MS, Pattash AC: Intranasal cocaine addiction. Lancet 1983;2:1374. 3. Cregler LL, Mark H: Medical complications of cocaine abuse. N Engl J Med 1986;315:1495-1500. 4. Waxman M: Sterile breast abscess in a heroin addict. Mt Sinai l Med 1978;45:738-741.
5. Eckland DA, Zeigler MG: Abscess in the nonlactating breast. Arch Surg 1973;107:398-401. 6. KilgoreAR, Fleming R: Abscessesof the breast: Recurringlesions in the areolar area. california Medicine 1952;77:190-191. 7. Weiss RL, Matsen JM: Group B streptococcal breast abscess. Arch Pathol Lab Med 1987;111:74-75. 8. Webb D, Thadepalli H: Skin and soft tissue polymicrobial infections from intravenous abuse of drugs. West J Med 1979;130:200-204. 9. Orangio GR, Pitlick SD, Latta PD, et al: Soft tissue infections in parenteral drug abusers. Ann Surg 1984;199:97-100. 10. Vilensky W: Illicit and licit drugs causing perforation of the nasal septurn. J Forensic Sci 1982;27:958-962.
Annals of Emergency Medicine
187/119
Ibuprofen Blood Levels Vary To the Editor: We welcomed the Hall et al article, "Ibuprofen Overdose: 126 Cases" [November 1986; 15:1308-1313] in its presentation of their nomogram and concise discussion of ibuprofen overdose symptomatology. We would like to add a sampling of four patients ingesting ibuprofen (and in w h o m levels were obtained) presenting to our emergency department within the previous six months. Case I. An 18-year-old, 70-kg w o m a n presented four hours after ingestion of 50 600-mg ibuprofen tablets {428 mg/kg). She was alert and asymptomatic. Her physical examination was unremarkable except for superficial lacerations over the volar aspects of her wrists. The patient's vital signs were blood pressure, 130/90 m m Hg; pulse, 76; respirations, 20; and afebrile. Treatment consisted of ipecac, activated charcoal with sorbitol, and tetanus-diphtheria toxoid. Toxicology screen five hours after ingestion demonstrated only ibuprofen at 38 ~g/mL. Serum electrolytes, BUN, and creatinine were all within normal limits. The patient remained asymptomatic and was transferred for psychiatric evaluation after six hours observation in the ED. Case 2. An 18-year-old, 75-kg man was transported to the ED after ingestion of 80 600-mg ibuprofen tablets (640 rag/ kg). The patient was obtunded, and responded only to noxious stimuli with combative behavior, without verbalization. Physical examination was otherwise remarkable only for nonreactive, 1-mm pupils. Vital signs were blood pressure, 120/60 m m Hg; pulse, 130; and respirations, 20. No response was noted with naloxone or DS0 W. The patient was intubated and paralyzed with vecuronium prior to gastric lavage and gastric installation of activated charcoal and sorbitol. Toxicology screen two hours after ingestion demonstrated ibuprofen level of 520 ~g/mL; ethanol, 106 mg%; and salicylates, 3.5 mg%. He remained intubated for 12 hours, and intermittent episodes of hypotension (systolic blood pressure, 80 to 100 mg Hg) were treated with isotonic fluid boluses. Subsequent ibuprofen levels at 4, 6.5, and 11.5 hours after ingestion were 320 p,g/mL, 124 ~g/mL, and 9.5 p,g/mL, respectively. Of note, this patient developed a severe hypophosphatemia (PO4, 0.8 mg/dL), as well as a hypokalemia {requiring 160 mEq KC1 IV over the first 12 hours to maintain K + at 3.6 mEq/L) following his ingestion. He was discharged six days after admission after noting a mild rise in AST (33 to 61 IU/L), ALT (30 to 80 IU/L) and LDH {207 to 386 IU/L), which subsequently resolved. Renal failure never developed. He developed chicken pox two days after admission.
Case 3. A 16-year-old, 55-kg girl presented two hours after ingestion of 28 600-mg ibuprofen tablets (305 mg/kg). She was alert with complaints of headache and tinnitus. Physical examination was unremarkable. Vital signs were blood pressure, 150/82 m m Hg; pulse, 118; respirations, 16; and afebrile. Treatment consisted of naloxone, ipecac, and activated charcoal with sorbitol. Toxicology screen at four hours after ingestion reported only ibuprofen at 37 ~g/mL. Serum electrolytes, BUN, and creatinine were all normal. The patient remained asymptomatic and was discharged after six hours of observation in the ED. Case 4. A 21-year-old woman presented one hour after ingestion of 20 800-mg ibuprofen tablets (200 mg/kg). She was alert and asymptomatic, with an unremarkable physical examination. Vital signs were blood pressure, 142/74 m m Hg; pulse, 92; respirations, 20; and afebrile. Treatment consisted of ipecac and activated charcoal with sorbitol. Toxicology screen two hours after ingestion demonstrated only trace ibuprofen in the blood. She remained asymptomatic, and was transferred for psychiatric evaluation after six hours of observation in the ED. These four cases demonstrate the variability of measured ibuprofen blood levels, reported a m o u n t s ingested, and syrnptomatology in adults; as such, they correlate well with the findings of Hall et al. Of interest is our second case, in which the patient developed a marked potassium and phosphate deficit following ingestion. There is no reason to suspect that this was due to either the other drugs he ingested or was iatrogenic in nature. These abnormalities have not been described previously in ibuprofen ingestions. Though the rise in AST, ALT, and LDH was minor, it is difficult to determine if this was sec o ondary to his ingestion or his exposure to varicella. These evaluations are not clinically signifieant and have been noted previously1, ~ in those taking normal quantities of ibuprofen, but not in single-dose ingestions. Fred Harchelroad Jr, MD Timothy C Evans, MD Elgin Hobbs, MD Division of Emergency Medicine Allegheny General Hospital Pittsburgh, Pennsylvania 1. Stempel DA, Miller JJ: Lymphopenia and hepatic toxicity with ibuprofen, l Pediatr 1977;90:657-658. 2. Royer GL, Seckman CE, Welshman IR: Safetyprofile: Fifteen years of clinical experiencewith ibuprofen. Am l Med 1984~77:25-34.
Cocaine Abuse and Unusual Injection Sites To the Editor: As the illicit use of cocaine has continued to increase, so too have cocaine-related emergency department visits, hospital admissions, and deaths.~ Cocaine is most often taken 118/186
mtranasally.Z It also may be injected subcutaneously, IM or IV; taken orally, vaginally, sublingually, or rectally; and may be smoked, a For the IV drug abuser, potential routes of ad-
Annals of Emergency Medicine
17:2 February 1988
ministration become harder to identify as superficial veins thrombose and sclerose. The use of the breast, a highly vascular and accessible organ, as the point of entry for drug injections is not well recognized by physicians. 4 We report a case of injection of cocaine into a superficial vein of the breast with resultant breast infection, septic shock, and death. A 45-year-old woman was seen in the ED of DC General Hospital one week after injecting cocaine into a superficial vein of the upper right breast. Five days earlier she had been evaluated in a walk-in clinic with a temperature of 38.9 C orally and vague somatic complaints. No breast abnormality was recognized and she was sent home. On physical examination the patient was afebrile. Vital signs were blood pressure, 72/40 m m Hg; respirations, 40; and pulse, 130. The patient was obese with large breasts. The right breast had a 10 cm x 6 cm dark superficial ulceration in the upper outer quadrant with a surrounding zone of erythema. The involved breast was not crepitant. Old needle tracts were seen over the legs, arms, and hands. Laboratory studies included a white blood cell count of 3,500/nlrn3; arterial blood gases on room air were pH, 7.33; PCO2, 26; and PO2, 57. Chest roentgenogram showed interstitial edema consistent with early adult respiratory distress syndrome. ECG revealed a sinus tachycardia. The patient was admitted to the M I C U w i t h a presumptive diagnosis of septic shock secondary to a breast infection. Increasing respiratory distress prompted endotracheal intubation and mechanical ventilatory support. D o p a m i n e started at 2.5 ~xg/kg/min was increased progressively to maintain a systolic blood pressure of 90 m m Hg. Fine-needle aspiration of the right breast did not demonstrate any significant fluid collection. G r a m stain of scant right breast aspirate revealed Gram-positive cocci. After blood, urine, and sputum cultures were obtained, IV antibiotics were started empirically (vancomycin hydrochloride 500 m g every six hours; clindamycin phosphate 600 mg every six hours; and a single dose of gentamicin 150 rag) and a surgical consultation was called. Before surgical intervention could be instituted the patient became bradycardic and suffered a cardiopulmonary arrest from which she could not be resuscitated. Approximately 12 hours after presentation to the ED she was pronounced dead. At autopsy, there was diffuse suppurative inflammation of the right breast, including the overlying s u b c u t a n e o u s tissue and underlying muscles of the right upper chest wall. This process extended just beyond the midline to the left. Microscopic sections of the breast confirmed an extensive suppurative inflammatory process. Abscess formation in the nonlactating breast is uncommon.S Etiologic factors include major duct disease, concomitant cutaneous infection elsewhere, and chronic illness known to predispose to infection (eg, diabetes mellitus). The most c o m m o n organism isolated from abscesses in the nonlactating breast is staphylococcus. 6 Breast abscesses caused by injection of illicit drugs should respond to treatment m u c h as localized suppuration elsewhere in the body. Incision and drainage or excision should result in satisfactory and lasting resolution of the inflam17:2 February 1988
matory process in a majority of cases. Antibiotic therapy is an important adjunct to the surgical procedure. Because staphylococci are the most c o m m o n infecting organisms, the empiric use of a penicillinase-resistant penicillin is advised.7 Soft tissue infections in illicit drug abusers are often polymicrobial. Webb and T h a d e p a l l i reported r e c o v e r y of anerobes in 14 of 21 patients (67%) with severe soft tissue infections, and advised initial therapy with clindamycin and an aminoglycoside.90rangio et al commonly recovered anerobes, enteric Gram-negative aerobes, and oropharyngeal organisms from a similar group of patients. They recommended a semisynthetic penicillin with an antistaphlococcal activity, such as nafcillin or oxacillin, combined with an aminoglycoside to cover the high incidence of Gram-negative enteric anerobes. 9 In our case, the site of injection of cocaine was unusual and the potential for life-threatening infection unrecognized. The local necrotizing effect of the drug was analogous to the effect of cocaine on the nasal septum in intranasal abusers and undoubtedly contributed to the extensive inflammatory process found within the breast.lo Although fine-needle aspiration did not suggest an undrained collection, the clinical setting and physical findings we described should prompt an early and aggressive incision and drainage procedure. Physicians need to be aware of the enormity of the threat that cocaine abuse represents in this country. Moreover, they need to recognize the stigmata of cocaine abuse, including injection of this drug into unusual sites such as the breast. R i c h a r d W Holt, M D D a n i e l L Miller, M D G e o r g e t o w n U n i v e r s i t y Surgical D i v i s i o n DC General Hospital Washington, DC
1. Gay ~R: Clinical management of acute and chronic cocaine poisoning.
Ann Emerg Med 1982;11:562-572.
2. Washton AM, Gold MS, Pattash AC: Intranasal cocaine addiction. Lancet 1983;2:1374. 3. Cregler LL, Mark H: Medical complications of cocaine abuse. N Engl J Med 1986;315:1495-1500. 4. Waxman M: Sterile breast abscess in a heroin addict. Mt Sinai l Med 1978;45:738-741.
5. Eckland DA, Zeigler MG: Abscess in the nonlactating breast. Arch Surg 1973;107:398-401. 6. KilgoreAR, Fleming R: Abscessesof the breast: Recurringlesions in the areolar area. california Medicine 1952;77:190-191. 7. Weiss RL, Matsen JM: Group B streptococcal breast abscess. Arch Pathol Lab Med 1987;111:74-75. 8. Webb D, Thadepalli H: Skin and soft tissue polymicrobial infections from intravenous abuse of drugs. West J Med 1979;130:200-204. 9. Orangio GR, Pitlick SD, Latta PD, et al: Soft tissue infections in parenteral drug abusers. Ann Surg 1984;199:97-100. 10. Vilensky W: Illicit and licit drugs causing perforation of the nasal septurn. J Forensic Sci 1982;27:958-962.
Annals of Emergency Medicine
187/119