Lucas, Charles E. MD, FACS
The use of illicit street narcotics has a major impact on many trauma center programs. Injury is caused by either the pharmaceutical effects or the mode of administration of these drugs. Although many drugs with varying effects are readily available, this treatise focuses on the injurious effects of the prime depressant heroin and the prime stimulant cocaine, as experienced in a large verified Level I inner-city trauma center.1–4
Heroin is derived from morphine, which is the principal product of the poppy Papaver somniferum. Heroin interacts with endogenous opiate receptors that function as neurotransmitters, neurohormones, and modulators of neurotransmission. Heroin-related injury includes overdose, soft-tissue infections, endocarditis, abscesses, vascular thromboses, vascular aneurysms, and solid-organ abscesses.2 When an injured patient is first seen in the trauma center, often family members or friends help identify heroin addiction by volunteering the patient’s history of drug use. Heroin addiction can also be recognized by physical signs of previous heroin injection (i.e., needle tracks, superficial venous thrombosis, and ‘skin pop’ scars at the sites of previous subcutaneous injections). Lymphedema with swollen extremities and associated cellulitis caused by lymphatic fibrosis may also be present. Knowledge of the patient’s heroin addiction can be particularly useful during an emergency operation. The anesthesiologist may need to administer large quantities of narcotics and muscle relaxants. The anesthesiologist may also encounter problems with oxygenation because of previous pulmonary embolization of talc and other particulates, which for profit motives, are used to dilute heroin before it is injected.
Overdose from Heroin
Users who are ignorant of injectate concentration run the greatest risk of overdosing. They often do not know the extent of heroin dilution unless their street distributors have developed an excellent reputation for consistency. Deaths from opiate overdose are caused by respiratory depression.2 Like morphine, heroin induces peripheral vasodilation and decreases systemic vascular resistance (further worsened by concomitant release of histamine). Any presence of alcohol aggravates the consequent hypotension. Reduction or prevention of heroin-related overdose might be possible with adequate knowledge or labeling of heroin concentration.
Infectious Complications of Heroin
Two prime contributors to infectious heroin-related injury are the method of injection and the bacterial contamination of the injectate. Many agents are used to dilute heroin including quinine, strychnine, lidocaine, sugars, talcum, and starch producing a product called ‘mixed jive.’ The diluents cause superficial venous sclerosis and thrombosis. The added bacterial seeding leads to thrombophlebitis and surrounding cellulitis. Once the peripheral lines are obliterated, larger veins or ‘main lines’ have to be used. When these main lines become thrombosed, the user resorts to subcutaneous injections or skin pops. Cellulitis and abscess frequently occur after skin popping. These infectious complications make it increasingly difficult for the user to successfully self-inject heroin. The user may resort to seeking help from street ‘doctors’ who make central injections into the internal jugular vein by way of a ‘pocket shot.’ Although these street doctors exhibit remarkable skill, there are associated complications, which include pneumothorax, tension pneumothorax, empyema, and cervical abscesses.
Abscesses from Heroin Use
During a 12-month interval, the surgeons at Detroit Receiving Hospital drained 421 abscesses associated with surrounding cellulitis caused by heroin or mixed-jive injections.5 Most abscesses occurred in the groin or leg, but some were present at all sites. The most common organism cultured from these abscesses was methicillin-resistant Staphylococcus aureus followed by beta hemolytic Streptococcus. Mixed flora was seen in 25% of patients. The average length of hospital stay was 12.4 days unless there were vascular complications, in which case, the average length of hospital stay increased to 26.3 days. The average hospital cost using 2003 estimates was $30,000 per patient.
A small percentage of these patients have widespread cellulitis and soft-tissue necrosis requiring extensive debridement of skin, subcutaneous tissue, and muscle.5,6 When performing extensive debridement, nerves should not be excised because they carry their own blood supply. Occasionally, the extent of rapidly spreading soft-tissue involvement requires four-quarter or hindquarter amputation to prevent rapid torso spread or death.6 Temporizing in this setting is fatal. Some patients with rapidly spreading soft-tissue involvement have negative cultures caused by an allergic reaction to foreign substances. For example, products, such as powdered skim milk, may have been injected deep into muscles to treat an overdose on the street.
Bacterial Resistance to Antimicrobials
The injectate often contains antimicrobials obtained from legal prescriptions written for other patients who were discharged after having had an abscess drained.2,5 This has resulted in a significant incidence of bacterial resistance to some important antimicrobial agents. Over the past 30 years, Detroit Receiving Hospital has repeatedly reported new antimicrobial resistance in heroin addicts.
Vascular Injuries from Heroin
Sometimes the user inadvertently punctures an artery because the presence of scarification and fibrosis from previous cellulitis makes successful intravenous injections more difficult.1,7 This usually causes a ‘pinky’ as red blood is withdrawn, requiring the needle to be removed without injection. Unfortunately the user may be incapacitated from associated alcohol or other substance abuse, not recognize the pinky, and inject the heroin intra-arterially. This causes severe burning of the distal part of the extremity because particulates from the injectate occlude the small vessels. Ischemia of fingers and toes or even hands and feet result. Tissues that are obviously necrotic require amputation; any viable adjacent tissues cause extensive pain. Aneurysmotomy occasionally must be followed by synthetic arterial graft replacement; recidivism inevitably leads to graft infection, thrombosis, and a threatened limb. Intra-arterial injection often leads to a perivascular hematoma, which becomes secondarily infected. The resulting abscess communicates through the injection site with the arterial lumen. This entity is called a mycotic aneurysm, a pseudonym for an infected pseudoaneurysm.7 During a 20-month interval, surgeons at Detroit Receiving Hospital excised 52 mycotic aneurysms in 50 addicts.
Venous aneurysms also occur in the heroin user.8 These are harder to diagnose because no pulse is transmitted, and the surrounding area typically displays cellulitis. The patient’s respiratory system is usually compromised because of the embolization of bacteria resulting in bilateral pneumonia. Microabscesses cause respiratory failure and often require ventilatory support. Anticoagulation in these patients has the potential for causing intracerebral bleeding because of unrecognized intracranial mycotic aneurysms.
Bacterial endocarditis is a major heroin-related injury. It resists therapy and consumes extensive hospital resources. Recurrent infection may complicate valvular replacement, which can be fatal. Refractory endocarditis is often associated with intrasplenic abscesses caused by bacterial embolization.9 Patients treated only with antibiotics typically develop recurrent infection, leading to death. Patients undergoing valvulotomy without valvular replacement are candidates for splenectomy performed simultaneously or subsequent to cardiac surgery. By removing the abscessed spleen, the likelihood of reinfection decreases.9
Infected Solid-Organ Hematomas
Frequently, intraparenchymal hematomas are observed after nonoperative treatment of patients suffering blunt liver and splenic injury.2 Heroin users may have bacterial seeding of the hematoma, which can become an abscess and require drainage.
Cocaine is derived from the coca plant Erythroxylum coca, which is easily grown in warm climates.3 Nicolas Monardes published the first known scientific paper on cocaine in 1565. The coca leaf used to produce cocaine was introduced from South America into Europe in 1580, where its cultivation flourished for the next three centuries.3 The United States became involved in the science of cocaine in 1854. A scientific team led by Pizzi established a lab at La Paz, Bolivia, and extracted the cocaine alkaloid. Niemann isolated the alkaloid from coca plant leaves and coined the name ‘cocaine.’ Cocaine use became popular as a topical anesthetic in the late 19th century when it was used for many minor operations. The lay public used cocaine to treat symptoms of runny nose, hay fever, and fatigue.3 Pemberton, in 1886, mixed the coca leaf extract with the African kola nut making syrup, which was later introduced into the soft drink Coca-Cola. In 1913, widespread use of cocaine in various forms led President Taft to declare cocaine ‘public enemy number 1.’ Congress then defined cocaine as a narcotic by passage of the Harrison Act in 1914. Cocaine use continued as part of an underground network for the next several decades until the early 1970s when inexpensive crack cocaine became widely available. This led to the current upsurge in cocaine use. Fifty million Americans have tried, or are currently using, cocaine; over half of injured patients presenting to inner-city trauma centers have used, or are using, cocaine.
Physiologic and Pathologic Effects
Physiologic cocaine-related injury is caused by intense vasoconstriction, which may affect both small and large vessels.10 In patients under 45 years of age, cocaine is the number one cause of stroke, fatal cardiac arrhythmia, and myocardial infarction.11,12 Patients with cocaine-related and concomitant injuries experience worse pulmonary insult. Vasoconstriction occurs, causing microscopic pulmonary infarcts. Hemorrhagic shock requiring multiple blood transfusions after an injury often leads to shock-lung syndrome, and respiratory function worsens as the need for ventilation support increases. Cocaine-related injury associated with vasoconstriction also increases renal vascular resistance, causing oliguric or nonoliguric renal failure.3,13 This condition is more likely to occur in patients receiving multiple transfusions.
Cocaine-related injury involves the gut. Acute perforation of a duodenal ulcer occurs shortly after cocaine inhalation. This results from focal ischemia in the proximal duodenum.3,14 Patients sustaining blunt abdominal injury may develop what appears to be an acute abdomen because of hollow viscous rupture. Laparotomy often reveals a focal peritoneal insult with a walled-off area of the small bowel or colon around a microscopic perforation.3,15 Histologic examination identifies the focal necrosis with submucosal inflammation, fibrosis, and small vessel thrombosis from cocaine, not blunt hollow viscus rupture. When seen after a motor vehicle collision or assault, the surgeon cannot distinguish between cocaine-induced ischemic injury and blunt hollow viscous perforation. Consequently, the laparotomy is nontherapeutic. Focal hepatic necrosis is also seen after cocaine exposure. Hepatocellular enzymes can reach very high levels.3
Intense vasoconstriction causes muscle ischemia progressing to compartment syndrome with or without associated long bone fractures.3 A cocaine-induced compartment syndrome causes more pain than typically seen after low-limb perfusion without cocaine. The extent of rhabdomyolysis is very high after cocaine-related injury. Compartment syndrome in patients with both hemorrhagic shock and cocaine exposure is likely to cause renal shutdown; the coexistent renal effects of cocaine contribute to renal failure.15
Cocaine-induced vasoconstriction may also cause thrombosis of large arteries.3 Examples include the abdominal aorta and the femoral, popliteal, iliac, and renal arteries.16 The intense constriction of blood flow in the vasovasorum leads to intimal damage. The point of intimal damage attracts platelets, which adhere to endothelium. Concurrently, cocaine enhances coagulation because it reduces the levels of protein-C and antithrombin-III.3,17,18 In turn, the induced platelet activation and aggregation promote fibrin deposition and large vessel thrombosis.
Injured patients on cocaine often are paranoid, uncooperative, and difficult to manage during the preoperative and postoperative phases.3 Paranoid ideation and bipolar behavior are typical of recent cocaine exposure. Restraints are often needed. The effects of cocaine on the central nervous system may impede use of the Glasgow Coma Scale score to evaluate the patient. When a patient recovers from the acute injury but unexpectedly dies, one should suspect illicit cocaine exposure and collect blood and urine samples for toxicology.19 Cocaine exposure also leads to spontaneous abortion, stillbirth, and other complications of pregnancy.3
One patient with cocaine-related injury after a motor vehicle collision is presented to highlight the way in which drug use complicates trauma management. A 34-year-old unrestrained man was drag racing on a major thoroughfare when he collided with two other vehicles. Two innocent people were killed, and three were badly injured. He was unconscious at the scene and was resuscitated, splinted, and transferred to the trauma center where he arrived at 12:39 am. He had stable vital signs and a Glasgow Coma Scale score of 12. Imaging studies showed multiple rib fractures, a midshaft femur fracture, which was splinted, and multiple contusions. A toxicology screen showed a blood alcohol content of 0.78 mg/dL and strong positivity for cocaine. (Alcohol is frequently used with cocaine to both blunt the high and prolong the euphoria.) He had intramedullary rodding of the femur at 2:00 am and went to the intensive care unit at 3:30 am, where he became acidotic and complained of pain in his right calf. Arteriography showed a large aortic thrombus, bilateral renal artery thrombi, and thrombotic occlusion of the right iliac, right profunda femoris, and left popliteal arteries. Immediate transabdominal thrombectomy of the aortic, renal, and iliac vessels was followed by exploration of the popliteal artery and extensive thrombectomy.
Postoperatively, he developed the expected complications of cocaine-related injury. He became confused and obtunded with a Glasgow Coma Scale score of 5. His pulmonary function deteriorated, requiring a tracheostomy and long-term ventilatory support. Then he progressed to renal shutdown—a condition associated with cocaine-induced rhabdomyolysis of several muscle groups (including both legs). Bilateral calf fasciotomies were needed to preserve limbs. He had coronary vasoconstriction with myocardial infarction, gut ischemia with prolonged adynamic ileus, hepatocellular dysfunction, and coagulopathy. Therapy included prolonged ventilation, hemodialysis, intravenous nutrition, and multiple antibiotics for the infectious complications. Gradually, his multiple organ dysfunctions improved. He was discharged to a rehabilitation center 90 days after his injury, showing normal mental and renal functions and assisted ambulation with crutches.
Preventive Measures: Reducing the Burden on Trauma Care
Heroin and cocaine have become readily available throughout the past 30 years. Drug-related injury from street narcotics is generally caused by ignorance of drug concentration or bacterial contamination from unsterile preparation. Often the drug-related injury is combined with another type of injury, such as a motor vehicle collision. This treatise has shown numerous ways in which illicit drug use, specifically heroin and cocaine use, complicates trauma care management and places an additional burden on the trauma center’s resources. If the American pharmaceutical industry were to legally prepare and distribute these agents, sterility and accurate labeling of drug concentrations would result. Bribery of our law enforcement agents for protecting an illicit drug industry would cease. The real war on drugs can only be successfully won through tax-funded education and rehabilitation. Generous taxation would support educational and rehabilitative programs.20 Pending such legislative changes, the most efficient way to prevent illicit drug recidivism would be to institute prevention programs in trauma centers. This is where patients who have used street drugs and ingested alcohol are initially treated for concomitant injuries, and this is where implementing preventive programs will yield the greatest medical consequences.
1. Lucas CE, Ledgerwood AM. Illicit street drugs and vascular injury. In: Rich N, Mattox KL, Hirschberg A, eds. Vascular Trauma. 2nd ed. Philadelphia, PA: W.B. Saunders; 2004:421–426.
2. Lucas CE, Ledgerwood AM, Kline RA. Alcohol and drugs. In: Mattox KL, Feliciano DV, Moore EE, eds. Trauma. New York, NY: McGraw-Hill; 2000:1059–1074.
3. Shanti CM, Lucas CE. Cocaine and the critical care challenge. Crit Care Med. 2003;31:1851–1859.
4. National Institute on Drug Abuse. National Household Study on Drug Abuse: Population Estimates 1998. Rockville, Md: National Institute on Drug Abuse, Division of Epidemiology and Statistical Analysis, US Department of Health and Human Services, Public Health Service, Alcohol, Drug Abuse, and Mental Health Administration; 1998.
5. Wallace JR, Lucas CE, Ledgerwood AM. Social, economic, and surgical anatomy of a drug-related abscess. Am Surg. 1986;52:398–401.
6. Vega JM, Lucas CE. Rapidly spreading subcutaneous inflammation after ‘skin popping’ in drug addicts. Am J Surg. 1979;45:392–393.
7. Johnson JR, Ledgerwood AM, Lucas CE. Mycotic aneurysm: new concepts in therapy. Arch Surg. 1983;118:577–582.
8. Johnson JR, Lucas CE, Ledgerwood AM, Jacobs LA. Infected venous psychoaneurysm: a complication of drug addiction. Arch Surg. 1984;119:1097–1098.
9. Robinson SL, Saxe JM, Lucas CE, Arbulu A, Ledgerwood AM, Lucas WF. Splenic abscess associated with endocarditis. Surgery. 1992;112:781–787.
10. Boghdadi MS, Henning RJ. Cocaine: pathophysiology and clinical toxicology. Heart Lung. 1997;26:466–481.
11. Aggrawal SK, Williams V, Levine SR, Casson BJ, Garcia JH. Cocaine associated intracranial hemorrhage: absence of vasculitis in 14 cases. Neurology. 1996;46:1741–1743.
12. Pitts WR, Lange RA, Cigarroa JE, Hillis LD. Cocaine induced myocardial ischemia and infarction: pathophysiology, recognition, and management. Prog Cardiovasc Dis. 1997;40:65–76.
13. Singhal PC, Rubin RB, Peters A, Santiago A, Neugarten J. Rhabdomyolysis and acute renal failure associated with cocaine abuse. J Toxicol Clin Toxicol. 1990;28:321–330.
14. Sharma R, Organ CH, Hirvela ER, Henderson VJ. Clinical observation of the temporal association between crack cocaine and duodenal ulcer perforation. Am J Surg. 1997;174:629–633.
15. Niazi M, Kondru A, Levy J, Bloom AA. Spectrum of ischemic colitis in cocaine users. Dig Dis Sci. 1997;42:1537–1541.
16. Webber J, Kline RA, Lucas CE. Aortic thrombosis associated with cocaine use: report of two cases. Ann Vasc Surg. 1999;13:302–304.
17. Heesch CM, Negus BH, Steiner M, et al. Effects of in vivo cocaine administration on human platelet aggregation. Am J Cardiol. 1996;78:237–239.
18. Moliterno DJ, Lange RA, Gerard RD, Willard JE, Lackner C, Hillis LD. Influence of intranasal cocaine on plasma constituents associated with endogenous thrombosis and thrombolysis. Am J Med. 1994;96:492–496.
19. Krome RL, Ledgerwood A, Lucas CE. The hazards of drug addiction on a trauma ward. Mich Med. 1971;70:603–605.
20. Tran M. Drug war is ‘futile exercise.’ Guardian Weekly. June 1998;21:5.
© 2005 Lippincott Williams & Wilkins, Inc.