- Email: [email protected]
Rhabdomyolysis: A late complication of near-drowning
CASE REVIEW
Rhabdomyolysis: A Late Complication of Near-drowning Author: Julie L. Lester, RN, CEN, Keller, Tex Section Editor: Anne Marie Lewis, RN, BSN, BA, MA, CEN
Julie L. Lester, Dallas Chapter, is Education Coordinator, Emergency Department, Baylor Medical Center, Irving, Texas; E-mail: [email protected]. Reprints not available from the author. J Emerg Nurs 2002;28:280-3. Copyright © 2002 by the Emergency Nurses Association. 0099-1767/2002 $35.00 +0 18/1/126235 doi:10.1067/men.2002.126235
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A
28-year-old Hispanic man came to the emergency department following a flight from Cancun, Mexico, where he had been hospitalized. Approximately 24 hours earlier, the patient had consumed a large quantity of alcohol and then went for a swim in the ocean. After 40 minutes, his friends reported him missing. During that time, he was struggling vigorously in ocean currents, his muscles began cramping, and he aspirated a moderate amount of salt water. The medical records from the Mexican hospital were translated and revealed that the patient had been rescued from the water and had spontaneous respiratory effort at the scene. On arrival at the local emergency department, his vital signs were as follows: blood pressure (BP), 150/70 mm Hg; pulse rate, 130 beats per minute; and respirations, 24 breaths per minute. He was cyanotic, with a pulse oximetry reading of 88% on room air, and was “hypothermic,” although his body temperature was not noted in the records. During the hospitalization, he received a “tranquilizer” for muscle pain, along with oxygen, antibiotics, and intravenous steroids. On the flight to the United States, the patient’s symptoms worsened. When he presented to our bilingual triage nurse, his chief complaint was “blood in urine and pain all over.” He also stated that he had had 4 episodes of “bloody diarrhea.” His vital signs were as follows: BP, 200/105 mm Hg; pulse rate, 78 beats per minute; respirations, 18 breaths per minute; and oral temperature, 37.6°C (99.7°F). His pulse oximetry reading was 99% on room air. He rated his generalized muscle pain as 8 out of 10. The triage nurse assigned him to an emergent acuity level. The patient’s initial assessment revealed a patent airway, no palpable neck tenderness, unlabored breathing, and warm, dry, pale skin with a capillary refill slightly greater
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TABLE 1
Initial laboratory values* (normal values) Arterial blood gas value
On O2 at 2 L/min via nasal cannula pH, 7.361 (7.35-7.45) PCO2, 24.8 L (35-45 mm Hg) PO2, 109.1 H (75-100 mm Hg) HCO3, 13.7 L (22-26 mmol/L) Cardiac enzymes
CPK, 334,224 H (24-61 U/L) (drawn 24 h after injury) (no MB available) CPK, 128,430 IU/L (drawn 8 h after treatment initiated) TropI, 0.8 H (0.0-0.3 ng/mL) CBC
WBC, 18.2 H (4.5-11/mm3) RBC, 4.9 (4.5-5.8 million/mm3) HGB, 15.8 (13-17.0 g/dL) HCT, 44.9 (40.0%-51.0%) Platelets, 207 (130-400/mm3) Chemistry
NA, 127 L (135-145 mEq/L) K, 6.1 H (3.5-5.1 mEq/L) K, 5.5 H (8 h after treatment initiated) CL, 96 L (98-107 mEq/L) CO2, 16 L (22-29 mEq/L) GLUC, 123 H (70-108 mg/dL) BUN, 48 H (7-18 mg/dL) (continued)
Chemistry (cont.)
Creatinine, 4.7 H (0.6-1.3 mg/dL) TP, 6.3 L (6.8-8.2 G/dL) ALB, 2.9 L (3.5-5.0 G/dL) T.BILI, 0.6 (0.0-1.0 mg/dL) CA, 7.3 L (8.8-10.5 mg/dL) Liver enzymes
SGOT, 9091 H (15-37 U/L) SGPT, 2041 H (7-40 U/L) PT/PTT
PT 14.0 H (11.4-13.1 sec) PTT 29.1 (24.6-33.7 sec) Urinalysis
WBC, 5-10/HPF RBC, 3-5/HPF Epithelial cells few/LPF Nitrite positive (neg) Crystals moderate/HPF (uric acid) Bacteria moderate/HPF Color amber GLUC 100 (neg mg/dL) BLOOD LARGE (neg) pH, 5.0 (5.0-8.0) Protein >300 Myoglobin >100 mg/dL
ALB, albumin; BUN, blood urea nitrogen; CA, calcium; CBC, complete blood cell count; CL, chloride; CO2, carbon dioxide; CPK, creatinine phosphokinase; GLUC, glucose; HCO3, bicarbonate; HCT, hematocrit; HGB, hemoglobin; HPF, high-power field; K, potassium; LPF, low-power field; NA, sodium; O2, oxygen; PCO2, partial pressure of carbon dioxide; PO2, partial pressure of oxygen; PT, prothrombin time; PTT, partial thromboplastin time; RBC, red blood cell count; SGOT, serum glutamate oxaloacetate transaminase; SGPT, serum glutamate; T.BILI, total bilirubin; TP, total protein; TropI, troponin I; WBC, white blood cell count. *Abnormal values are in italics.
than 2 seconds. Auscultation of the chest revealed bibasilar coarse rales. The cardiac monitor showed normal sinus rhythm without ectopy. His Glasgow Coma Scale score was 15, and his pupils were equal and reactive. His abdomen was nondistended with active bowel sounds, but he complained of generalized abdominal tenderness on palpation. He also reported nausea, without vomiting. Although he was able to move all 4 extremities, he complained of severe muscle pain with minimal palpation. Pulses were present in all extremities. There were no obvious signs of trauma. After the emergency physician’s examination, we established an intravenous line of 0.9% normal saline solution
and infused it at 150 mL per hour. Results of an EKG were normal, but the patient’s chest radiograph showed bilateral infiltrates. Insertion of a urinary catheter returned only 30 mL of “tea-colored” urine that tested positive for blood. We administered ceftriaxone, 1 g intravenously, for the pneumonia, and the patient’s nausea was treated successfully with promethazine (Phenergan), 12.5 mg, administered intravenously. At this time, the patient reported increasing “stiffness,” and he had decreased range of motion. Based on his laboratory results (Table 1), we suspected that the patient might have rhabdomyolysis and acute renal failure (ARF). We initiated alkalinization therapy by adding
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100 mEq of an 8.4% concentration of sodium bicarbonate to a liter of dextrose and 0.45% normal saline (D51⁄2NS) solution. The infusion rate was maintained at 150 mL per hour. We also administered furosemide (Lasix), 100 mg intravenously, famotidine (Pepcid), 20 mg intravenously, sodium polystyrene sulfonate (Kayexalate), 30 g orally, and vitamin K, 10 units subcutaneously. During the subsequent hours of ED treatment, the patient’s BP remained elevated, with a systolic reading between 150 and 160 mm Hg and a diastolic reading between 100 and 110 mm Hg. An arterial blood gas sample obtained 3 hours after the initiation of alkalinization therapy indicated a compensated metabolic acidosis (Table 1). The patient was transferred to ICU with a diagnosis of rhabdomyolysis, ARF, aspiration pneumonia, early disseminated intravascular coagulation (DIC), and acute hepatic failure.
Our patient’s “tea-colored” urine was caused by myoglobin. However, myoglobin will not always be present because it may disappear from the plasma within 6 hours of injury.3 The patient’s initially elevated creatinine and blood urea nitrogen levels correlate with a 70% to 85% reduction in glomerular filtration rate. In the presence of both hypovolemia and aciduria (pH < 5.6), myoglobin becomes toxic and uric acid tends to crystallize.4 Intravenous sodium bicarbonate is recommended to alkalinize the urine.3 This medication should be titrated to maintain a urine pH of 7.0.3
He presented with all of the hallmark signs of the condition: myalgias, stiffness, weakness, malaise, low-grade fever, and dark brown urine.
Our patient had rhabdomyolysis, one of the late complications of neardrowning.1 He presented with all of the hallmark signs of the condition: myalgias, stiffness, weakness, malaise, low-grade fever, and dark brown urine. In this case, it occurred after excessive alcohol intake, probable hypothermia, and vigorous muscular activity related to the near-drowning struggle. Rhabdomyolysis involves injury to the skeletal muscles, causing potentially toxic cellular contents to leak into the systemic circulation.2 We observed the typical clinical sequelae in our patient: hypovolemia from sequestration of plasma within injured myocytes, hyperkalemia from release of cellular potassium into the systemic circulation, metabolic acidosis from release of cellular phosphate and sulfate, ARF from the nephrotoxic effects of liberated myocytes in renal tubules, and DIC from thromboplastin that is released from injured myocytes.2 Measuring the patient’s serum creatine phosphokinase (CPK) level makes the definitive diagnosis of rhabdomyolysis. Patients with CPK levels in excess of 5 times the normal level who also have associated risk factors for rhabdomyolysis should have a complete work-up performed.3 Serum CPK levels generally peak within 24 hours and then should decrease by approximately 40% per day (Table 1).
Aggressive intravenous hydration during the first 24 to 72 hours is the cornerstone of treatment for rhabdomyolysis. Support of the intravascular volume increases the glomerular filtration rate and dilutes myoglobin and other renal tubular toxins. Rapid initiation of isotonic crystalloids at 500 mL per hour is recommended, and the fluids should be titrated to maintain a urine output of 200 to 300 mL per hour.5 During our patient’s 4 hours in the emergency department, his total urinary output was a mere 200 mL, while his intake of intravenous fluids was 800 mL. His initial intravenous infusion of 0.9% normal saline solution should have been continued rather than changing it to the hypertonic D51⁄2NS solution. This may have contributed to his low urine output. Injured myocytes can sequester large volumes of extracellular fluids and crystalloid requirements can be quite high, as much as 20 L in the first 24 hours after the injury.4 However, our patient was hypertensive because of the activation of the renin-angiotensin system and the sodium retention of his ARF. Consequently, we had to do a careful balancing act to prevent fluid overload, which can occur in oliguric ARF, yet still provide the necessary intravascular volume to dilute his myoglobin. Our patient’s potassium level was moderately elevated at 6.1 mEq/L. He was treated promptly with intravenous sodium bicarbonate to alkalinize the serum (and urine)
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pH. This treatment caused a temporary shift of potassium from the extracellular to the intracellular compartment. In addition, diuretics were initiated with high-dose furosemide (100 mg every 6 hours) to promote renal excretion of potassium. Lastly, binding resin therapy (Kayexalate) was provided to remove potassium through the gastrointestinal tract.
We had to do a careful balancing act to prevent fluid overload, which can occur in oliguric ARF, yet still provide the necessary intravascular volume to dilute his myoglobin. The elevated white blood cell (WBC) count and lowgrade temperatures between 37.6°C and 38.1°C (99.7° and 100.6° F) indicated that our patient was becoming septic. In addition to the aspiration pneumonia on his chest radiograph, the patient’s urinalysis revealed a probable urinary tract infection. We started antibiotic treatment promptly. Our patient’s bloody diarrhea was explained by the fact that, during a drowning incident, blood is shunted away from the gastrointestinal tract and diverted to the brain, heart, and muscles. Widespread sloughing of the gut may result.6 His findings of DIC (ie, bloody diarrhea and possibly the hematuria), with his prolonged prothrombin time of 14.0 seconds, prompted the administration of vitamin K. He had no more episodes of bloody diarrhea after receiving the histamine H2 -receptor antagonist famotidine.
REFERENCES 1. Chopra K. Near-drowning. Hospital Reviews 1996;147:7-14. 2. Craig S. Rhabdomyolysis. eMedicine J [serial online] 1998;3(1). Available from: URL: http://www.emedicine.com/emerg/ traumaandorthopedics/topic508/htm 3. Counselman F. Rhabdomyolysis. In: Tintinalli J, Ruiz E, Krome R, editors. Emergency medicine: a comprehensive study guide. New York: McGraw Hill; 1996. p. 1841-5. 4. Sinert R, Kohl L, Rainone T, Scalea T. Exercise induced rhabdomyolysis. Ann Emerg Med 1994;23:1301. 5. Gabow PA, Kaehny WD, Kelleher SP. The spectrum of rhabdomyolysis. Medicine (Baltimore) 1982;61:141. 6. Knopp R. Near-drowning. In: Tintinalli J, Ruiz E, Krome R, editors. Emergency medicine: a comprehensive study guide. New York: McGraw Hill; 1996. p. 1013-8. This section features actual emergency situations with particular educational value for the emergency nurse. Contributions (4 to 6 typed, double-spaced pages) should include a case summary focused on the emergency care phase, accompanied by pertinent case commentary. Submit to: Anne Marie Lewis, RN, BSN, BA, MA, CEN, Section Editor, c/o Managing Editor, PO Box 489, Downers Grove, IL 60515 800 900-9659, ext 4044 • [email protected]
Conclusion
During the first 24 hours, our patient remained oliguric with a urine output of 400 mL per day. There was minimal improvement in his serial blood urea nitrogen and creatinine studies. After 24 hours in the ICU, he began hemodialysis. Normal kidney function resumed after the fourth dialysis treatment. After 9 days, he was discharged home. Acknowledgment Special thanks to Eryc Nieto, Triage RN, and Minerva Santos, ED technician, for the translation of case records.
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Rhabdomyolysis: A Late Complication of Near-drowning Author: Julie L. Lester, RN, CEN, Keller, Tex Section Editor: Anne Marie Lewis, RN, BSN, BA, MA, CEN
Julie L. Lester, Dallas Chapter, is Education Coordinator, Emergency Department, Baylor Medical Center, Irving, Texas; E-mail: [email protected]. Reprints not available from the author. J Emerg Nurs 2002;28:280-3. Copyright © 2002 by the Emergency Nurses Association. 0099-1767/2002 $35.00 +0 18/1/126235 doi:10.1067/men.2002.126235
280
A
28-year-old Hispanic man came to the emergency department following a flight from Cancun, Mexico, where he had been hospitalized. Approximately 24 hours earlier, the patient had consumed a large quantity of alcohol and then went for a swim in the ocean. After 40 minutes, his friends reported him missing. During that time, he was struggling vigorously in ocean currents, his muscles began cramping, and he aspirated a moderate amount of salt water. The medical records from the Mexican hospital were translated and revealed that the patient had been rescued from the water and had spontaneous respiratory effort at the scene. On arrival at the local emergency department, his vital signs were as follows: blood pressure (BP), 150/70 mm Hg; pulse rate, 130 beats per minute; and respirations, 24 breaths per minute. He was cyanotic, with a pulse oximetry reading of 88% on room air, and was “hypothermic,” although his body temperature was not noted in the records. During the hospitalization, he received a “tranquilizer” for muscle pain, along with oxygen, antibiotics, and intravenous steroids. On the flight to the United States, the patient’s symptoms worsened. When he presented to our bilingual triage nurse, his chief complaint was “blood in urine and pain all over.” He also stated that he had had 4 episodes of “bloody diarrhea.” His vital signs were as follows: BP, 200/105 mm Hg; pulse rate, 78 beats per minute; respirations, 18 breaths per minute; and oral temperature, 37.6°C (99.7°F). His pulse oximetry reading was 99% on room air. He rated his generalized muscle pain as 8 out of 10. The triage nurse assigned him to an emergent acuity level. The patient’s initial assessment revealed a patent airway, no palpable neck tenderness, unlabored breathing, and warm, dry, pale skin with a capillary refill slightly greater
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TABLE 1
Initial laboratory values* (normal values) Arterial blood gas value
On O2 at 2 L/min via nasal cannula pH, 7.361 (7.35-7.45) PCO2, 24.8 L (35-45 mm Hg) PO2, 109.1 H (75-100 mm Hg) HCO3, 13.7 L (22-26 mmol/L) Cardiac enzymes
CPK, 334,224 H (24-61 U/L) (drawn 24 h after injury) (no MB available) CPK, 128,430 IU/L (drawn 8 h after treatment initiated) TropI, 0.8 H (0.0-0.3 ng/mL) CBC
WBC, 18.2 H (4.5-11/mm3) RBC, 4.9 (4.5-5.8 million/mm3) HGB, 15.8 (13-17.0 g/dL) HCT, 44.9 (40.0%-51.0%) Platelets, 207 (130-400/mm3) Chemistry
NA, 127 L (135-145 mEq/L) K, 6.1 H (3.5-5.1 mEq/L) K, 5.5 H (8 h after treatment initiated) CL, 96 L (98-107 mEq/L) CO2, 16 L (22-29 mEq/L) GLUC, 123 H (70-108 mg/dL) BUN, 48 H (7-18 mg/dL) (continued)
Chemistry (cont.)
Creatinine, 4.7 H (0.6-1.3 mg/dL) TP, 6.3 L (6.8-8.2 G/dL) ALB, 2.9 L (3.5-5.0 G/dL) T.BILI, 0.6 (0.0-1.0 mg/dL) CA, 7.3 L (8.8-10.5 mg/dL) Liver enzymes
SGOT, 9091 H (15-37 U/L) SGPT, 2041 H (7-40 U/L) PT/PTT
PT 14.0 H (11.4-13.1 sec) PTT 29.1 (24.6-33.7 sec) Urinalysis
WBC, 5-10/HPF RBC, 3-5/HPF Epithelial cells few/LPF Nitrite positive (neg) Crystals moderate/HPF (uric acid) Bacteria moderate/HPF Color amber GLUC 100 (neg mg/dL) BLOOD LARGE (neg) pH, 5.0 (5.0-8.0) Protein >300 Myoglobin >100 mg/dL
ALB, albumin; BUN, blood urea nitrogen; CA, calcium; CBC, complete blood cell count; CL, chloride; CO2, carbon dioxide; CPK, creatinine phosphokinase; GLUC, glucose; HCO3, bicarbonate; HCT, hematocrit; HGB, hemoglobin; HPF, high-power field; K, potassium; LPF, low-power field; NA, sodium; O2, oxygen; PCO2, partial pressure of carbon dioxide; PO2, partial pressure of oxygen; PT, prothrombin time; PTT, partial thromboplastin time; RBC, red blood cell count; SGOT, serum glutamate oxaloacetate transaminase; SGPT, serum glutamate; T.BILI, total bilirubin; TP, total protein; TropI, troponin I; WBC, white blood cell count. *Abnormal values are in italics.
than 2 seconds. Auscultation of the chest revealed bibasilar coarse rales. The cardiac monitor showed normal sinus rhythm without ectopy. His Glasgow Coma Scale score was 15, and his pupils were equal and reactive. His abdomen was nondistended with active bowel sounds, but he complained of generalized abdominal tenderness on palpation. He also reported nausea, without vomiting. Although he was able to move all 4 extremities, he complained of severe muscle pain with minimal palpation. Pulses were present in all extremities. There were no obvious signs of trauma. After the emergency physician’s examination, we established an intravenous line of 0.9% normal saline solution
and infused it at 150 mL per hour. Results of an EKG were normal, but the patient’s chest radiograph showed bilateral infiltrates. Insertion of a urinary catheter returned only 30 mL of “tea-colored” urine that tested positive for blood. We administered ceftriaxone, 1 g intravenously, for the pneumonia, and the patient’s nausea was treated successfully with promethazine (Phenergan), 12.5 mg, administered intravenously. At this time, the patient reported increasing “stiffness,” and he had decreased range of motion. Based on his laboratory results (Table 1), we suspected that the patient might have rhabdomyolysis and acute renal failure (ARF). We initiated alkalinization therapy by adding
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100 mEq of an 8.4% concentration of sodium bicarbonate to a liter of dextrose and 0.45% normal saline (D51⁄2NS) solution. The infusion rate was maintained at 150 mL per hour. We also administered furosemide (Lasix), 100 mg intravenously, famotidine (Pepcid), 20 mg intravenously, sodium polystyrene sulfonate (Kayexalate), 30 g orally, and vitamin K, 10 units subcutaneously. During the subsequent hours of ED treatment, the patient’s BP remained elevated, with a systolic reading between 150 and 160 mm Hg and a diastolic reading between 100 and 110 mm Hg. An arterial blood gas sample obtained 3 hours after the initiation of alkalinization therapy indicated a compensated metabolic acidosis (Table 1). The patient was transferred to ICU with a diagnosis of rhabdomyolysis, ARF, aspiration pneumonia, early disseminated intravascular coagulation (DIC), and acute hepatic failure.
Our patient’s “tea-colored” urine was caused by myoglobin. However, myoglobin will not always be present because it may disappear from the plasma within 6 hours of injury.3 The patient’s initially elevated creatinine and blood urea nitrogen levels correlate with a 70% to 85% reduction in glomerular filtration rate. In the presence of both hypovolemia and aciduria (pH < 5.6), myoglobin becomes toxic and uric acid tends to crystallize.4 Intravenous sodium bicarbonate is recommended to alkalinize the urine.3 This medication should be titrated to maintain a urine pH of 7.0.3
He presented with all of the hallmark signs of the condition: myalgias, stiffness, weakness, malaise, low-grade fever, and dark brown urine.
Our patient had rhabdomyolysis, one of the late complications of neardrowning.1 He presented with all of the hallmark signs of the condition: myalgias, stiffness, weakness, malaise, low-grade fever, and dark brown urine. In this case, it occurred after excessive alcohol intake, probable hypothermia, and vigorous muscular activity related to the near-drowning struggle. Rhabdomyolysis involves injury to the skeletal muscles, causing potentially toxic cellular contents to leak into the systemic circulation.2 We observed the typical clinical sequelae in our patient: hypovolemia from sequestration of plasma within injured myocytes, hyperkalemia from release of cellular potassium into the systemic circulation, metabolic acidosis from release of cellular phosphate and sulfate, ARF from the nephrotoxic effects of liberated myocytes in renal tubules, and DIC from thromboplastin that is released from injured myocytes.2 Measuring the patient’s serum creatine phosphokinase (CPK) level makes the definitive diagnosis of rhabdomyolysis. Patients with CPK levels in excess of 5 times the normal level who also have associated risk factors for rhabdomyolysis should have a complete work-up performed.3 Serum CPK levels generally peak within 24 hours and then should decrease by approximately 40% per day (Table 1).
Aggressive intravenous hydration during the first 24 to 72 hours is the cornerstone of treatment for rhabdomyolysis. Support of the intravascular volume increases the glomerular filtration rate and dilutes myoglobin and other renal tubular toxins. Rapid initiation of isotonic crystalloids at 500 mL per hour is recommended, and the fluids should be titrated to maintain a urine output of 200 to 300 mL per hour.5 During our patient’s 4 hours in the emergency department, his total urinary output was a mere 200 mL, while his intake of intravenous fluids was 800 mL. His initial intravenous infusion of 0.9% normal saline solution should have been continued rather than changing it to the hypertonic D51⁄2NS solution. This may have contributed to his low urine output. Injured myocytes can sequester large volumes of extracellular fluids and crystalloid requirements can be quite high, as much as 20 L in the first 24 hours after the injury.4 However, our patient was hypertensive because of the activation of the renin-angiotensin system and the sodium retention of his ARF. Consequently, we had to do a careful balancing act to prevent fluid overload, which can occur in oliguric ARF, yet still provide the necessary intravascular volume to dilute his myoglobin. Our patient’s potassium level was moderately elevated at 6.1 mEq/L. He was treated promptly with intravenous sodium bicarbonate to alkalinize the serum (and urine)
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Discussion
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pH. This treatment caused a temporary shift of potassium from the extracellular to the intracellular compartment. In addition, diuretics were initiated with high-dose furosemide (100 mg every 6 hours) to promote renal excretion of potassium. Lastly, binding resin therapy (Kayexalate) was provided to remove potassium through the gastrointestinal tract.
We had to do a careful balancing act to prevent fluid overload, which can occur in oliguric ARF, yet still provide the necessary intravascular volume to dilute his myoglobin. The elevated white blood cell (WBC) count and lowgrade temperatures between 37.6°C and 38.1°C (99.7° and 100.6° F) indicated that our patient was becoming septic. In addition to the aspiration pneumonia on his chest radiograph, the patient’s urinalysis revealed a probable urinary tract infection. We started antibiotic treatment promptly. Our patient’s bloody diarrhea was explained by the fact that, during a drowning incident, blood is shunted away from the gastrointestinal tract and diverted to the brain, heart, and muscles. Widespread sloughing of the gut may result.6 His findings of DIC (ie, bloody diarrhea and possibly the hematuria), with his prolonged prothrombin time of 14.0 seconds, prompted the administration of vitamin K. He had no more episodes of bloody diarrhea after receiving the histamine H2 -receptor antagonist famotidine.
REFERENCES 1. Chopra K. Near-drowning. Hospital Reviews 1996;147:7-14. 2. Craig S. Rhabdomyolysis. eMedicine J [serial online] 1998;3(1). Available from: URL: http://www.emedicine.com/emerg/ traumaandorthopedics/topic508/htm 3. Counselman F. Rhabdomyolysis. In: Tintinalli J, Ruiz E, Krome R, editors. Emergency medicine: a comprehensive study guide. New York: McGraw Hill; 1996. p. 1841-5. 4. Sinert R, Kohl L, Rainone T, Scalea T. Exercise induced rhabdomyolysis. Ann Emerg Med 1994;23:1301. 5. Gabow PA, Kaehny WD, Kelleher SP. The spectrum of rhabdomyolysis. Medicine (Baltimore) 1982;61:141. 6. Knopp R. Near-drowning. In: Tintinalli J, Ruiz E, Krome R, editors. Emergency medicine: a comprehensive study guide. New York: McGraw Hill; 1996. p. 1013-8. This section features actual emergency situations with particular educational value for the emergency nurse. Contributions (4 to 6 typed, double-spaced pages) should include a case summary focused on the emergency care phase, accompanied by pertinent case commentary. Submit to: Anne Marie Lewis, RN, BSN, BA, MA, CEN, Section Editor, c/o Managing Editor, PO Box 489, Downers Grove, IL 60515 800 900-9659, ext 4044 • [email protected]
Conclusion
During the first 24 hours, our patient remained oliguric with a urine output of 400 mL per day. There was minimal improvement in his serial blood urea nitrogen and creatinine studies. After 24 hours in the ICU, he began hemodialysis. Normal kidney function resumed after the fourth dialysis treatment. After 9 days, he was discharged home. Acknowledgment Special thanks to Eryc Nieto, Triage RN, and Minerva Santos, ED technician, for the translation of case records.
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