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Massive Pulmonary Edema in a Habitual Crack Cocaine Smoker Not Chemically Positive for Cocaine at the Time of Surgery

1997; Lippincott Williams & Wilkins; Volume: 84; Issue: 5 Linguagem: Inglês

10.1213/00000539-199705000-00041

1526-7598

D. J. Bird, James R. Markey,

Neuroscience of respiration and sleep

The acute, deleterious effects of illicit cocaine use are well documented [1-6]. The physiologic effects of cocaine result in a state of excessive sympathetic stimulation with resultant hypertension, tachycardia, vasoconstriction, agitation, mydriasis, and a predisposition to arrhythmias. Previous review articles [1] and case reports [2] have described the cardiopulmonary consequences of acute cocaine usage. The problems encountered intraoperatively in acutely intoxicated users have also been described [3]. Hypertension and pulmonary edema after induction of anesthesia in patients who tested positive for cocaine and were known to have taken it recently have been described [2,3]. We were, however, unable to find a description in the literature of a chronic user, not acutely intoxicated, who suffered tachycardia, hypertension, and pulmonary edema, as previously described for acute intoxication. We report a case of sudden, profound hypertension and pulmonary edema after uneventful induction of general anesthesia in a clandestine, habitual, crack cocaine smoker who had not used cocaine for several days prior to surgery. Case Report A 34-yr-old man was scheduled for internal mandibular fixation for a fracture sustained in a fall 10 days earlier. The patient admitted to heavy alcohol use and cigarette smoking of one to two packs a day for 15 yr, but he specifically denied any personal history of hypertension, heart disease, asthma, or illicit drug usage. He had no allergies. The patient had undergone an uncomplicated incision and drainage of a facial abscess under general anesthesia in 1994. Upon physical examination, he appeared as a thin, relaxed 167-cm, 68-kg man. Blood pressure (BP) was 105/63 mm Hg, heart rate (HR) was 76 bpm, respiratory rate (RR) was 20 breaths/min, and temperature was 36.8 degrees C oral. Significant physical findings included a supple neck with full range of motion; however, mandibular range of motion was limited to 20 mm. His lungs were clear, and heart sounds were regular without murmur. Complete blood count and serum electrolytes were normal except for a hemoglobin count of 11.5 g/dL. Sickle cell prep was negative. Preoperative electrocardiogram and chest radiographs were normal. The patient was premedicated with ranitidine 150 mg per os (PO), metaclopramide 10 mg PO, and sodium citrate 0.3 mM, 30 mL PO the morning of surgery. In the operating room, the electrocardiogram, pulse oximeter, and blood pressure cuff were placed, and initial vital signs were BP 130/70 mm Hg, and HR was 95 bpm. The patient was given fentanyl 150 micro g and midazolam 2 mg intravenously (IV) and was prepared for awake nasal fiberoptic intubation. Four drops of 1% phenylepherine nasal solution were placed in the nares, and 4% lidocaine-soaked swabs were placed in the nasal passages. Superior and laryngeal nerve blocks were completed with 1% lidocaine. Fiberoptic nasal intubation was quick and uneventful, and the patient remained calm without coughing or bucking. His airway was patent at all times. Placement of the endotracheal tube was confirmed with capnography, auscultation, and fiberoptic inspection. Anesthesia was induced with thiopental 400 mg IV, and ventilation was controlled with RR 10 breaths/min and tidal volume 700 mL with peak airway pressures of 26 cm H2 O. Anesthesia was maintained with sevoflorane 2.5% in oxygen. Throughout this period, the patient remained hemodynamically stable with oxygen saturation of more than 97%. Attempted placement of a Foley catheter was difficult and prolonged due to operator inexperience, and BP precipitously increased to 250/150 mm Hg with a HR of 150 bpm. The sevoflorane concentration was increased from 2.5% to 5%, and Foley insertion was stopped. Fentanyl 350 g and labetalol 20 mg were given with the BP decreasing to 170/100 mm Hg and a HR of 100 bpm. Pulse oximetry decreased from 100% to 88% despite a fraction of inspired oxygen (FiO2) of 1.0. Breath sounds revealed coarse rales bilaterally, and suctioning of the endotracheal tube returned 150 mL of serosanguinous fluid. A presumptive diagnosis of pulmonary edema was made, and positive end-expiratory pressure of 10 cm H2 O was initiated. Over the next 20 min, a total of 750 mL of fluid was suctioned from the endotracheal tube. Fluid administration to this point was 400 mL of lactated Ringer's solution. Arterial blood gas results were pHA 7.29, PaCO2 56 mm Hg, PaCO2 89 mm Hg, and CO (2) 26 mEq/L, despite a minute ventilation of 7.0 L/min and an FiO2 of 1.0. An arterial line and pulmonary artery catheter were inserted to help guide management. The initial central venous pressure was 1 mm Hg, pulmonary artery pressure was 25/15 mm Hg, the pulmonary capillary wedge pressure was 12 mm Hg, and the cardiac output was 6.2 L/m. Lactated Ringer's solution, 2500 mL, was required to increase the BP to 100/70 mm Hg with a central venous pressure of 6 mm Hg and a pulmonary capillary wedge pressure of 15 mm Hg. A chest radiograph in the operating room showed an appropriately placed endotracheal tube with well-expanded lungs and bilateral air bronchograms. There were no cutaneous signs or wheezing. Surgery was canceled, and the patient was transferred to the recovery room, where he was sedated and mechanically ventilated. There he remained hemodynamically stable, and follow-up chest radiographs demonstrated fluffy, bilateral infiltrates and vascular redistribution consistent with the diagnosis of pulmonary edema. Serial cardiac enzymes (CPK-MB) were negative, all electrocardiogram results remained normal, and a bedside echocardiogram was consistent with normal left ventricular function. His urine was negative for vanillylmandelic acid and metanephrines. The patient diuresed spontaneously and was tracheally extubated 4 h postoperatively. At that time, the patient was asked about illicit drug use again, and he admitted to smoking crack cocaine several times a week for the last 3 yr. His most recent usage had been 3 days prior to surgery. Serum and urine samples were analyzed for illicit drugs and found to be negative for cocaine or other drugs. Discussion Cocaine is the most frequently abused controlled substance in the United States [4]. Estimates of regular users approach six million [5]. The trend from nasally insufflating cocaine hydrochloride to "freebasing" the cocaine alkaloid is increasing due to the significant reduction in user cost and the immediacy of the effects. Cocaine is an ester local anesthetic with sympathomimetic properties. The systemic effects of cocaine are predominantly a result of its ability to block the presynaptic reuptake of the neurotransmitters norepinephrine and dopamine. It is this "amplification" of the sympathetic nervous system that produces euphoria, tachycardia, hypertension, agitation, mydriasis, and a predisposition to arrhythmias. Stimuli that result in sympathetic activation under these conditions produce profoundly exaggerated responses. The immediate complications of cocaine use include tachycardia and hypertension [6], tachyarrhthmias [7,8], angina pectoris, myocardial infarction [7,8], and sudden death [9]. The pulmonary complications of smoking crack cocaine manifest as pulmonary edema [10,11], hemorrhage [12], pneumothorax [13], interstitial pneumonitis [14], and exacerbations of asthma [15]. Pulmonary edema has been seen in users of all forms of cocaine, including IV [16], but is particularly prevalent in those who smoke crack cocaine. Cucco et al. [17] suggest that the etiologic basis for this is damage to the pulmonary capillary endothelium with transient left ventricular dysfunction either due to ischemia or to severe peripheral vasoconstriction from intense sympathetic activation. Alternatively, the alveolar epithelium may be directly injured by the inhalation of toxic substances with the subsequent involvement of the alveolar basement membrane [18], both of which are supported by the impaired pulmonary diffusion of carbon dioxide seen in these patients. Although the acute effects of crack cocaine have been described, there is very little written about the chronic effects and what the clinical implications of this drug may be. Susskind et al. [19] demonstrated increased lung permeability after long-term use of crack cocaine. Murray et al. [20] found pulmonary artery hypertrophy, pulmonary edema, and pulmonary hemorrhage in autopsy studies of patients who died of cocaine overdose. There are no reports of a toxicologically negative patient developing such profound hemodynamic instability and pulmonary edema as we experienced in our case. Our patient had an unexpected and severe hypertensive response to a moderate stimulus (Foley placement), which may suggest a chronic state of sympathetic nervous system impairment that persists after the drug can no longer be detected in the body. The tremendous volume of fluid suctioned from the endotracheal tube is consistent with the alveolar capillary permeability changes previously described in crack smokers. The hemodynamic data we were able to obtain shortly after the hypertensive episode were consistent with a very sudden hypertensive episode resulting in pulmonary edema. The time delay (20 minutes) between the placement of nasal phenylephrine and the hypertensive episode make a primary phenylepherine reaction unlikely. In conclusion, the cardiopulmonary complications previously described in acutely intoxicated patients are a persistent problem that may occur in chronic users who are drug-free at the time of surgery.