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Overwhelming s. pneumonia meningitis after basilar skull fracture: A case report
BRIEF REPORT
Overwhelming S. Pneumonia Meningitis after Basilar Skull Fracture: A Case Report Fred A. Severyn, MD, FACEP, 1 James Fenn, RN, CEN, N R E M T - P 1
1. Life Flight, St. Vincent Mercy Medical Center and Medical College Hospital, Toledo, Ohio Address for correspondence: Fred A. Severyn, MD, FACEP, Denver Health Medical Center, 777 Bannock St., Mailcode 3652, Denver, CO 80204-4507 Copyright © 2000 by Air Medical Journal Associates 1067-991X/2000/$8.00 + 0 Reprint no, 74/1/108561 doi: 10.1067/mmj.2000.108561
Introduction The air medical transport of victims with a closed head injury (CHD is a frequent mission for most transport programs. These patients ultimately benefit from transport to trauma centers where comprehensive neurosurgical management aimed at optimizing cerebral perfusion and decreasing intracranial pressure is integrated into the optimum care of the polytrauma patient. Most patients are victims of acute head injury; however, occasionally patients are transferred for treatment of CHI complications, secondary insults from medical therapy, or complications from the initial trauma itself. Life Flight is a rotor-wing air medical program jointly sponsored by St. Vincent Mercy Medical Center (SVMMC) and the Medical College of Ohio, based in Toledo, Ohio. The service flies two Dauphin 365N-1 aircraft, and the medical crew configuration is physician/nurse. Life Flight currently responds to more than 1700 missions annually, serving the northwest Ohio and southeastern Michigan region.
a volunteer basic life support EMS service. The patient had complained of earache for several days before becoming confused and then actively seizing. On EMS arrival, he alternated between active seizure activity and postictal combativeness; Life Flight subsequently was called out. When the flight crew arrived at the patient's residence, the combative patient was being restrained by the EMS crew to prevent further injury to himself. Initial patient report was an otherwise healthy 48-year-old man with no seizure history, no current medications, and a remote history of a fall 3 weeks before that had resulted in a head injury but no loss of consciousness. The flight crew nasotracheally intubated and hyperventilated the patient and established an intravenous line. The patient received midazolam (Versed), dextrose, and vecuronium (Norcuron) by IV and then was transferred to SVMMC without any h e m o d y n a m i c problems during transport.
Purpose The intention of this article is to report a complex case of delayed CHI complications that eventually resulted in the patient's death and discuss and review the pathophysiology and treatment options involved in the patient's care.
Hospital Care In the ED, the patient was noted to be febrile (39.1 Foley temperature), nonpurposeful and moving all extremities, and hemodynamically stable. His pupils were equal and reactive, with random eye m o v e m e n t s noted and no papilledema detected on fundoscopy. No meningeal signs were present, but a dull, bulging purple tympanic membrane was noted on the left and an upgoing toe on Babinski examination.
Air Medical Care Life Flight was dispatched to a scene for an unresponsive seizure patient in a nearby rural community served only by 102
July-September 2000 19:3 Air Medical Journal
:igure 2 CT Scan of Spheno-Ethmoidal
Baseline laboratories were obtained (the results are listed in Table 1), including blood cultures, and the patient was given 2 g ceftriaxone (Rocephin) and started on 1 g vancomycin before transport to CT scan. The CT scan was remarkable for pneumocephalus, shown in Figure 1, without any obliteration of the quadrageminal cisterns and without any acute blood or mass effect. Air fluid levels also were detected in the ethmoid and sphenoid sinuses, as can be seen in Figure 2. On arrival back in the ED, the patient underwent a careful lumbar puncture in the lateral decubitus position, and the results were significant for subjectively elevated opening pressure, leukocytosis in the cerebrospinal fluid (CSF), and a positive gram stain. Table 2 lists these and other results. Although the patient was admitted to the infectious disease (ID) and medical services, an ICU bed was
not immediately available because the hospital had a surplus of ICU patients. The patient continued to receive supportive therapy, including hyperventilation, maintenance fluids, sedation, antipyretics, and ID-consultant recommended decadron while in the ED. Approximately 6 hours after he arrived at the hospital, the patient suffered a cardiopulmonary arrest with initial asystole, then ventricular dysrrhythmias, pulseless electrical activity, and an eventual perfusing sinus rhythm. Thirty minutes after resuscitation the patient's urine output increased dramatically, exceeding 400 mL every 15 minutes. Urinary output was matched to IV fluid intake; the patient was given 1-deamino-8-D-arginine vasopressin and eventually went to an ICU bed, where he continued to be unstable the next day. An MRI scan showed no anatomical evidence for herniation, but evidence in-
Fable 2 Cerebrospinal Fluid Results
table • Baseline Laboratory Summary WBC Increased bands noted Glucose Lactic acid ABG
35,000 78 7.0 7.09/32/228
RBC WBC 97% neutrophils Protein Glucose Negative bacterial antigens Gram positive diplococci
Air Medical Journal 19:3 July-September 2000
550 5379 632 < 20
dicated gross cerebral edema and lack of cerebral blood flow. The patient subsequently failed an apnea test, was declared brain dead, and was removed from venfilatory support after an extensive discussion between the family and the admitring service. Autopsy results confirmed the acute meningitis with a dural laceration associated with a cribriform plate fracture and a fracture involving the nasoethmoidal complex. CSF and blood cultures ultimately were positive for pneumococcus with sensitivities showing resistance to ampicillin and penicillin. Additional history obtained later from the family after ICU admission revealed that the patient had fallen from a truck bed 3 weeks earlier without any loss of consciousness. A week later he complained of "sinus congestion" and had been taking nonprescribed samples of doxycycline and ampicillin for this condition. The "sinus congestion" did not improve, and the patient developed a left earache 3 days before his seizure onset.
Discussion The patient described here suffered a basilar skull fracture at the time of the initial fall. Dural disruptions frequently are associated with basilar skull and sinus fractures. Accompanying these dural disruptions are transient CSF fistulas that occur in 16% to 24% of adults with basilar skull fractures. 1 Almost certainly this patient's "sinus congestion" indeed was CSF rhinorrhea. As a complication, the CSF fistula not only drains out CSF but allows bacteria, air, and sinus contents to gain entry into the fluid itself in a retrograde fashion. Pneumocephalus has the same clinical implication as a CSF fistula. 1 The incidence of meningitis in the setting of CSF fistula is 7% to 35%, with mortality rates of 20% to 50%.1 The complications of meningitis associated with CSF fistulas are many: 20% of patients develop seizures, and 5% to 10% of survivors develop profound neurologic sequelae) The routine use of antibiotics does not favorably alter the incidence of meningitis and actually may favor the growth of antibiotic-resistant strains and fungal organisms. 2 This phenomenon is complicated further by the organisms t h e m s e l v e s b e c a u s e m o s t major 103
pathogens causing meningitis in this setring are encapsulated bacteria, 3 which, by their very nature, are harder to eradicate in a disease state. The final etiology in our patient was the classic Streptococcus pneumonia, an encapsulated organism that was penicillin-resistant in this case. Penicillin resistance in S. pneumonia infections is on the rise in the United States, and our base hospital's incidence is 30%.4 The bacterial proliferation in the CSF initiates a wide range of pathophysiologic changes in the CNS and widespread changes associated with sepsis once the organism enters the bloodstream. The body's basic defense systems cause an intense influx of cells to fight off the organism, and the mediators released can cause further secondary brain injury by vasospasm and altered cerebral autoregulation. Paraspinal lymphatics not only can become obstructed, but absorption of the CSF itself can decrease as a result of cellular debris. 5 These combine to give rise to elevated intracranial pressure. Nutrient supply and utilization in the CSF also are disrupted, and falls in the CSF glucose very commonly are noted. Appropriate treatment of the bacterial infection includes empiric antibiotic therapy aimed at eradicating the most likely organisms. Unfortunately, the bacterial lysis and destruction itself triggers an intense inflammatory response that can lead to increased brain edema and further clinical decompensation. 5 For this reason, many clinicians are advocat-
ing the use of intravenous steroids in combination with antibiotic administration as the standard of care. 6 The human body has many regulatory systems, and the regulation of osmolarity is one of the most tightly controlled physiological parameters. Despite huge variations in water intake, fluid loss, and solute ingestion, the osmolarity maintains stability. This regulation occurs predominately through the actions of antidiuretic hormones (ADH), whose effect on the distal renal tubules is the ability to concentrate urine and conserve water balance. 5 ADH is synthesized in the supraoptic and paraventricular nuclei of the hypothalamus and transported by long axons from these nuclei to the posterior pituitary. 7 Significant hypothalamic or brainstem injury disrupts ADH secretion, resulting in the eventual inability to concentrate urine, clinically described as diabetes insipidus (D1). DI is characterized by the production of large volmnes (more than 300 to 400 mL per hour) of hypotonic urine. 8 Accurate replacement of fluid deficits is critically important, as well as attempts to slow the process of DI if fluid losses cannot be replaced effectively. Today's changing paradigm of neurosurgical critical care is aimed at optimizing cerebral perfusion pressure, providing adequate oxygenation and nutrition, and limiting intracranial hypertension. 9 The loss of large volumes of diluted urine quickly shifts intravascular volume into a hypovolemic state if allowed to continue. Frequent urinary output mea-
Air medical services routinely provide medical care and transport acutely ill and injured patients, ultimately decreasing morbidity and improving survival for the population served. Medical crews should be aware of the potential complications of seemingly minor injuries; by understanding the disease process and associated pathophysiology, they can better treat this subset of patients. The unfortunate patient described here suffered a simple basilar skull fracture with a delayed cerebrospinal fistula that resulted in bacterial meningitis. The infection was identified promptly and treated aggressively, but a succession of disease-related complications ensued. Despite aggressive medical care, the virulence of the organism, the overwhelming sepsis, and the intense inflammatory response to the meningitis itself ultimately caused the patient's death.
4. St. Vincent Mercy Medical Center Microbiology Laboratory. Antibiotic susceptibility report, January-December 1997. Toledo (OH): The Center; 1997. 5. Stein J. Internal medicine. Boston : Little, Brown and Company; 1990. p. 1281-91. 6. Gilbert D, Moellering R, Sande M. The Sanford guide to antimicrobial therapy. Vienna (VA):
Antimicrobial Therapy, Inc.; 1998. 7. Nolte J. The human brain. St. Louis: CV Mosby; 1981. p. 186. 8. Rosen P, Barkin R. Emergency medicine. St. Louis: Moshy; 1998. p. 2434-5. 9. Brain Trauma Foundation. Guidelines for the management of severe head injury. New York: The Foundation; 1995.
surements combined with fluid replacement are critical in maintaining cerebral perfusion. Replacing ADH through pitressin or desmopressin acetate (DDAVP) can restore disrupted osmolarity regulation that occurs in DI and help restore homeostasis. If the DI episode is transient, the use of longer-acting DDAVP theoretically can result in a rebound state of excess water retention with resulting edema; therefore, careful monitoring of intake, output, and metabolic paramet e r s - s u c h as electrolytes, renal function, and osmolarity--is crucial. Conclusion
References 1. Maull K, Rodriguez A, Wiles C. Complications in trauma and critical care. Philadelphia: WB Sannders; 1996. p. 201-13. 2. Ignelzi R, VanderArk G. Analysis of treatment of basilar skull fractures with and without antibiotics. J Neurosurg 1975;43:721-66. 3. Keroack M. The patient with suspected meningifts. Emerg Med Clin North Am 1987;5:807-26.
104
July-September 2000 19:3 Air Medical Journal
Overwhelming S. Pneumonia Meningitis after Basilar Skull Fracture: A Case Report Fred A. Severyn, MD, FACEP, 1 James Fenn, RN, CEN, N R E M T - P 1
1. Life Flight, St. Vincent Mercy Medical Center and Medical College Hospital, Toledo, Ohio Address for correspondence: Fred A. Severyn, MD, FACEP, Denver Health Medical Center, 777 Bannock St., Mailcode 3652, Denver, CO 80204-4507 Copyright © 2000 by Air Medical Journal Associates 1067-991X/2000/$8.00 + 0 Reprint no, 74/1/108561 doi: 10.1067/mmj.2000.108561
Introduction The air medical transport of victims with a closed head injury (CHD is a frequent mission for most transport programs. These patients ultimately benefit from transport to trauma centers where comprehensive neurosurgical management aimed at optimizing cerebral perfusion and decreasing intracranial pressure is integrated into the optimum care of the polytrauma patient. Most patients are victims of acute head injury; however, occasionally patients are transferred for treatment of CHI complications, secondary insults from medical therapy, or complications from the initial trauma itself. Life Flight is a rotor-wing air medical program jointly sponsored by St. Vincent Mercy Medical Center (SVMMC) and the Medical College of Ohio, based in Toledo, Ohio. The service flies two Dauphin 365N-1 aircraft, and the medical crew configuration is physician/nurse. Life Flight currently responds to more than 1700 missions annually, serving the northwest Ohio and southeastern Michigan region.
a volunteer basic life support EMS service. The patient had complained of earache for several days before becoming confused and then actively seizing. On EMS arrival, he alternated between active seizure activity and postictal combativeness; Life Flight subsequently was called out. When the flight crew arrived at the patient's residence, the combative patient was being restrained by the EMS crew to prevent further injury to himself. Initial patient report was an otherwise healthy 48-year-old man with no seizure history, no current medications, and a remote history of a fall 3 weeks before that had resulted in a head injury but no loss of consciousness. The flight crew nasotracheally intubated and hyperventilated the patient and established an intravenous line. The patient received midazolam (Versed), dextrose, and vecuronium (Norcuron) by IV and then was transferred to SVMMC without any h e m o d y n a m i c problems during transport.
Purpose The intention of this article is to report a complex case of delayed CHI complications that eventually resulted in the patient's death and discuss and review the pathophysiology and treatment options involved in the patient's care.
Hospital Care In the ED, the patient was noted to be febrile (39.1 Foley temperature), nonpurposeful and moving all extremities, and hemodynamically stable. His pupils were equal and reactive, with random eye m o v e m e n t s noted and no papilledema detected on fundoscopy. No meningeal signs were present, but a dull, bulging purple tympanic membrane was noted on the left and an upgoing toe on Babinski examination.
Air Medical Care Life Flight was dispatched to a scene for an unresponsive seizure patient in a nearby rural community served only by 102
July-September 2000 19:3 Air Medical Journal
:igure 2 CT Scan of Spheno-Ethmoidal
Baseline laboratories were obtained (the results are listed in Table 1), including blood cultures, and the patient was given 2 g ceftriaxone (Rocephin) and started on 1 g vancomycin before transport to CT scan. The CT scan was remarkable for pneumocephalus, shown in Figure 1, without any obliteration of the quadrageminal cisterns and without any acute blood or mass effect. Air fluid levels also were detected in the ethmoid and sphenoid sinuses, as can be seen in Figure 2. On arrival back in the ED, the patient underwent a careful lumbar puncture in the lateral decubitus position, and the results were significant for subjectively elevated opening pressure, leukocytosis in the cerebrospinal fluid (CSF), and a positive gram stain. Table 2 lists these and other results. Although the patient was admitted to the infectious disease (ID) and medical services, an ICU bed was
not immediately available because the hospital had a surplus of ICU patients. The patient continued to receive supportive therapy, including hyperventilation, maintenance fluids, sedation, antipyretics, and ID-consultant recommended decadron while in the ED. Approximately 6 hours after he arrived at the hospital, the patient suffered a cardiopulmonary arrest with initial asystole, then ventricular dysrrhythmias, pulseless electrical activity, and an eventual perfusing sinus rhythm. Thirty minutes after resuscitation the patient's urine output increased dramatically, exceeding 400 mL every 15 minutes. Urinary output was matched to IV fluid intake; the patient was given 1-deamino-8-D-arginine vasopressin and eventually went to an ICU bed, where he continued to be unstable the next day. An MRI scan showed no anatomical evidence for herniation, but evidence in-
Fable 2 Cerebrospinal Fluid Results
table • Baseline Laboratory Summary WBC Increased bands noted Glucose Lactic acid ABG
35,000 78 7.0 7.09/32/228
RBC WBC 97% neutrophils Protein Glucose Negative bacterial antigens Gram positive diplococci
Air Medical Journal 19:3 July-September 2000
550 5379 632 < 20
dicated gross cerebral edema and lack of cerebral blood flow. The patient subsequently failed an apnea test, was declared brain dead, and was removed from venfilatory support after an extensive discussion between the family and the admitring service. Autopsy results confirmed the acute meningitis with a dural laceration associated with a cribriform plate fracture and a fracture involving the nasoethmoidal complex. CSF and blood cultures ultimately were positive for pneumococcus with sensitivities showing resistance to ampicillin and penicillin. Additional history obtained later from the family after ICU admission revealed that the patient had fallen from a truck bed 3 weeks earlier without any loss of consciousness. A week later he complained of "sinus congestion" and had been taking nonprescribed samples of doxycycline and ampicillin for this condition. The "sinus congestion" did not improve, and the patient developed a left earache 3 days before his seizure onset.
Discussion The patient described here suffered a basilar skull fracture at the time of the initial fall. Dural disruptions frequently are associated with basilar skull and sinus fractures. Accompanying these dural disruptions are transient CSF fistulas that occur in 16% to 24% of adults with basilar skull fractures. 1 Almost certainly this patient's "sinus congestion" indeed was CSF rhinorrhea. As a complication, the CSF fistula not only drains out CSF but allows bacteria, air, and sinus contents to gain entry into the fluid itself in a retrograde fashion. Pneumocephalus has the same clinical implication as a CSF fistula. 1 The incidence of meningitis in the setting of CSF fistula is 7% to 35%, with mortality rates of 20% to 50%.1 The complications of meningitis associated with CSF fistulas are many: 20% of patients develop seizures, and 5% to 10% of survivors develop profound neurologic sequelae) The routine use of antibiotics does not favorably alter the incidence of meningitis and actually may favor the growth of antibiotic-resistant strains and fungal organisms. 2 This phenomenon is complicated further by the organisms t h e m s e l v e s b e c a u s e m o s t major 103
pathogens causing meningitis in this setring are encapsulated bacteria, 3 which, by their very nature, are harder to eradicate in a disease state. The final etiology in our patient was the classic Streptococcus pneumonia, an encapsulated organism that was penicillin-resistant in this case. Penicillin resistance in S. pneumonia infections is on the rise in the United States, and our base hospital's incidence is 30%.4 The bacterial proliferation in the CSF initiates a wide range of pathophysiologic changes in the CNS and widespread changes associated with sepsis once the organism enters the bloodstream. The body's basic defense systems cause an intense influx of cells to fight off the organism, and the mediators released can cause further secondary brain injury by vasospasm and altered cerebral autoregulation. Paraspinal lymphatics not only can become obstructed, but absorption of the CSF itself can decrease as a result of cellular debris. 5 These combine to give rise to elevated intracranial pressure. Nutrient supply and utilization in the CSF also are disrupted, and falls in the CSF glucose very commonly are noted. Appropriate treatment of the bacterial infection includes empiric antibiotic therapy aimed at eradicating the most likely organisms. Unfortunately, the bacterial lysis and destruction itself triggers an intense inflammatory response that can lead to increased brain edema and further clinical decompensation. 5 For this reason, many clinicians are advocat-
ing the use of intravenous steroids in combination with antibiotic administration as the standard of care. 6 The human body has many regulatory systems, and the regulation of osmolarity is one of the most tightly controlled physiological parameters. Despite huge variations in water intake, fluid loss, and solute ingestion, the osmolarity maintains stability. This regulation occurs predominately through the actions of antidiuretic hormones (ADH), whose effect on the distal renal tubules is the ability to concentrate urine and conserve water balance. 5 ADH is synthesized in the supraoptic and paraventricular nuclei of the hypothalamus and transported by long axons from these nuclei to the posterior pituitary. 7 Significant hypothalamic or brainstem injury disrupts ADH secretion, resulting in the eventual inability to concentrate urine, clinically described as diabetes insipidus (D1). DI is characterized by the production of large volmnes (more than 300 to 400 mL per hour) of hypotonic urine. 8 Accurate replacement of fluid deficits is critically important, as well as attempts to slow the process of DI if fluid losses cannot be replaced effectively. Today's changing paradigm of neurosurgical critical care is aimed at optimizing cerebral perfusion pressure, providing adequate oxygenation and nutrition, and limiting intracranial hypertension. 9 The loss of large volumes of diluted urine quickly shifts intravascular volume into a hypovolemic state if allowed to continue. Frequent urinary output mea-
Air medical services routinely provide medical care and transport acutely ill and injured patients, ultimately decreasing morbidity and improving survival for the population served. Medical crews should be aware of the potential complications of seemingly minor injuries; by understanding the disease process and associated pathophysiology, they can better treat this subset of patients. The unfortunate patient described here suffered a simple basilar skull fracture with a delayed cerebrospinal fistula that resulted in bacterial meningitis. The infection was identified promptly and treated aggressively, but a succession of disease-related complications ensued. Despite aggressive medical care, the virulence of the organism, the overwhelming sepsis, and the intense inflammatory response to the meningitis itself ultimately caused the patient's death.
4. St. Vincent Mercy Medical Center Microbiology Laboratory. Antibiotic susceptibility report, January-December 1997. Toledo (OH): The Center; 1997. 5. Stein J. Internal medicine. Boston : Little, Brown and Company; 1990. p. 1281-91. 6. Gilbert D, Moellering R, Sande M. The Sanford guide to antimicrobial therapy. Vienna (VA):
Antimicrobial Therapy, Inc.; 1998. 7. Nolte J. The human brain. St. Louis: CV Mosby; 1981. p. 186. 8. Rosen P, Barkin R. Emergency medicine. St. Louis: Moshy; 1998. p. 2434-5. 9. Brain Trauma Foundation. Guidelines for the management of severe head injury. New York: The Foundation; 1995.
surements combined with fluid replacement are critical in maintaining cerebral perfusion. Replacing ADH through pitressin or desmopressin acetate (DDAVP) can restore disrupted osmolarity regulation that occurs in DI and help restore homeostasis. If the DI episode is transient, the use of longer-acting DDAVP theoretically can result in a rebound state of excess water retention with resulting edema; therefore, careful monitoring of intake, output, and metabolic paramet e r s - s u c h as electrolytes, renal function, and osmolarity--is crucial. Conclusion
References 1. Maull K, Rodriguez A, Wiles C. Complications in trauma and critical care. Philadelphia: WB Sannders; 1996. p. 201-13. 2. Ignelzi R, VanderArk G. Analysis of treatment of basilar skull fractures with and without antibiotics. J Neurosurg 1975;43:721-66. 3. Keroack M. The patient with suspected meningifts. Emerg Med Clin North Am 1987;5:807-26.
104
July-September 2000 19:3 Air Medical Journal