MUSCLES
Myoglobinuria The
Importance of Intensive Care and Peritoneal Dialysis
Elfrid
ACUTE
with Acute Renal Failure in Children
Cifuentes, M.D., Michael E. Norman, M.D., M. William Schwartz, M.D., Bruce Maley, LCDR, MC, USN, William Bason, CAPT, MC, USN
NECROSIS of muscle
lead disturbelectrolyte myoglobinuria, ances, acute renal failure, and even death. Early diagnosis and early treatment are of the utmost importance for a satisfactory recovery. There have been few reports of myoglobinuria with acute renal failure in the pediatric l~iterature.1-2 We here describe two children who illustrate the fulminant and lifethreatening potentialities of this syndrome, and the reversibility of acute renal failure with early peritoneal dialysis. to
can
severe
Case Reports Case 1 An eight-year-old black girl was transferred the US Naval Hospital of Philadelphia in February 1974. Her illness began four days prior to admission, with symptoms of an upper respiratory tract infection (cough and rhinitis), followed
to
From The Children’s
Hospital of Philadelphia and Department of Pediatrics, US Naval Hospital, Philadelphia, Pa. Correspondence to Michael E. Norman, M.D., The Children’s Hospital of Philadelphia, 34th Street and Civic Center Boulevard, Philadelphia, Pa. 19104. the
The views expressed herein are those of the authors and are not to be construed as official or as reflecting the views of the United States Navy or the Department of Defense.
severe bilateral anterior thigh pain. She had history of fever, nausea or vomiting, exposure to drugs, or chemicals. On admission to another hospital, physical and laboratory examinations were unrevealing except for a hematocrit of 46
by
no
Her urine was dark yellow with 4+ moderate glucose, a strongly positive o-toluidine test for occult blood, and one or two red blood cells per high power field but no casts. Over the next two and one-half days, anorexia, vomiting, lethargy, and somnolence were progressive. She exhibited delusional behavior. Urine output decreased and the color turned dark brown. Physical examination on transfer revealed a comatose child, with no auscultable or palpable blood pressure. She had Kussmaul-type respirations, with peripheral cyanosis and dilated pupils, and no spontaneous movements. The muscles were diffusely edematous. Laboratory reports were as follows: serum sodium 122 mEq/1, potassium 9.0 mEq/1, chloride 70 mEq/1, C02 18 mM/I; BUN 36 mg/dl; creatinine 3.4 mg/dl; calcium 7.2 mg/dl; phosphorus 11.3 mg/dl; lactic dehydrogenase 2,282 LU.lml, and creatinine phosphokinase 8,820 l.U./ml. Cultures of blood, urine, stool, and cerebrospinal fluid (CSF) were all negative. An EKG showed changes compatible with marked hyperkalemia. The urine was positive for myoglobin by spectrophotometry (600 and 800 m>)3 and by a hemagglutination inhibition test.**
per
cent.
protein,
*
Niyotel,
Ames
Company, Elkhart,
Ind.
63
Downloaded from cpj.sagepub.com at UCSF LIBRARY & CKM on March 22, 2015
The patient responded to treatment for shock and hyperkalemia, but a tracheostomy with artificial ventilation was needed for respiratory paralysis. Peritoneal dialysis was required because of azotemia and fluid overload from total anuria; this lasted for seven days. Diuresis commenced on the 14th hospital day. At the time of discharge, physical examination, muscle enzyme levels, and renal function were within normal limits.
associated with extreme muscular exertion. 1,2,4 A relationship to antecedent viral (e.g., gastrointestinal, respiratory) infections has been suggested but remains un-
Case 2
primary myopathy, seizures, drug overdose, or unusual exertion to explain muscle necrosis. A muscle biopsy in Case 2 revealed no virus-like particles, giant cells, or inclusion
proven. 2,6-8 In our two patients, rhabdomyolysis developed after upper respiratory tract infections, and progressed rapidly to anuric renal failure. Neither had evidence of trauma,
black girl was brought to The Hospital of Philadelphia with a sevenday history of upper respiratory tract infection, fever, vomiting, and progressive muscle pain A
13-year-old
Children’s
and weakness. She
was
in
acute
distress with
thready peripheral pulse (140/min)
bodies. The striking feature of our two cases was the complete anuria lasting one week, a distinctly unusual occurence in children with acute parenchymal renal failure from any cause. The alternative diagnosis of bilateral
a
and weak
respiratory effort (28/min). Blood pressure readings were unobtainable. Temperature was 38 C. She had diaphoresis and muscle tenderness and weakness over the thighs and lower extremities. Blood hemoglobin was 15.1 gznldl, hematocrit 42.9 per cent, leukocyte count 33,900/mm3, with 95 per cent neutrophils, and 5 per cent lymphocytes ; serum sodium 124 mEq/1, potassium 7.7 mEq/1, chloride 84 mEq/1, C02 11 mMll; BUN 39 mg/dl, creatinine 10.0 mg/dl; phosphorus 10.2 mgldl, calcium 5.0 mg/dl, glucose 180 mg/dl; SGOT 1,850 I.U./ml, SGPT 620 I.U./ml, lactic dehydrogenase 45,200 1. U./ml, and creatinine phosphokinase 100,000 to 269,000 l.U./ml. CSF and blood cultures were negative. treated with intravenous albumin, fluids, and hydrocortisone. No urine was passed after hydration and a single intravenous dose of mannitol. Bladder catheterization produced a few milliliters of dark brown urine; specific gravity was 1.025, protein 3+, glucose 2+, occult blood 3+ without red blood cells, and 3 to 5 white blood cells per high power field. No casts were seen, but the ammonium sulfate precipitation and hemagglutination inhibition tests (Myotel) were positive for myoglobin. Intermittent peritoneal dialysis was carried out for one week because of azotemia, hyperkalemia, and fluid overload secondary to complete anuria. Diuresis commenced on the eighth hospital day. Percutaneous renal biopsy revealed acute tubular necrosis with myoglobin casts. Biopsy of the left quadriceps muscle 15 weeks after the acute illness revealed nonspecific changes; no virus-like particles, giant cells, or inclusion bodies were seen. An ischemic exercise test was normal, with a threefold rise in venous lactate after one minute of ischemia. The patient made a full recovery.
She
Prompt institution of peritoneal dialysis is important because it is in the first three to five days that life-threatening hyperkalemia tends to occur.
was
Discussion
Myoglobinuria with acute renal failure is infrequent in childhood and is usually un-
.
renal cortical necrosis was considered with both children, since each presented to the hospital in shock, but their subsequent full recoveries made this diagnosis unlikely. A rental biopsy in Case 2 demonstrated acute tubular necrosis with myoglobin casts, hence it must be assumed that anuria resulted from the renal toxicity of heme pigment. Grossman, et al. have recently reviewed the theories to explain renal failure in heme pigmenturia.9 These include: 1) tubular plugging with myoglobin casts, 2) a primary decrease in glomular filtration rate, 3) direct nephrotoxicity with back diffusion into the circulation through damaged tubular epithelium, and 4) shunting of blood away from the cortex, with decreased glomular filtration. None of these theories alone seems to sufficiently explain the acute renal failure. Well-documented cases of acute tubular necrosis after exercise-induced myoglobinuria are rare.10 Nontraumatic rhabdomyolysis as the cause was 5 per cent in a large series of adults with acute renal failure reported by Grossman, et at.99
64
Downloaded from cpj.sagepub.com at UCSF LIBRARY & CKM on March 22, 2015
The
causes
globinuria globinuria
are
of myoglobinemia and myodiverse (Table 1). When myo-
is recurrent, a primary myopathy should be searched for. Because of the differences in protein binding and renal clearance, in myoglobinuria unlike hemoglobinuria the plasma may be normally colored. Mechanisms underlying myoglobinuria have recently been reviewed by Rowland and Penn. 11 Idiopathic rhabdomyolysis with myoglobinuria must be suspected whenever a child with fever, muscle pain, tenderness, weakness, and edema passes red or brown urine which gives a positive test for occult blood. Red blood cells of course are absent from the urine. Myoglobin may be differentiated from hemoglobin by a variety of techniques.~4 Spectrophotometry, readily available in most clinical laboratories, has traditionally been the standard method of identification. Technical problems, however, limit its usefulness. More sensitive techniques are immunologic in nature, and include polyacrylamide gel electrophoresis, immunodiffusion, 10.12 and the specific hemagglutination inhibition assay used with our patients. Pigmented granular casts do not differentiate myoglobinuria from hemoglobinuria (in the very small quantities of urine passed by our patients,
pigmented granular
casts were not
seen).
Necrosis of striated or cardiac muscle is reflected in elevation of muscle enzyme levels in serum. Serum glutamic oxaloacetic trans-
aminase, serum glutamic pyruvic transaminase, creatinine phosphokinase, and lactic
dehydrogenase were all strikingly elevated in patients. In addition, leakage of intracellular muscle constituents (e.,~., creatinine, potassium, phosphorus) into the circulation produces characteristic and striking elevations of serum levels of creatinine, potassium, and phosphate. Hypocalcemia often appears. An important additional clue to the diagnosis our
when
renal failure occurs is the disproportionate rise in serum creatinine and resultant lowered BUN: creatinine ratio
TABLE 1. Causes
of Myoglobinemia and Myoglobinuria
management of these
complications dramatically improved. Both of our patients recovered completely despite initial shock followed by complete anuria. Prompt institution of peritoneal dialysis is important because it is in the first three to five days, that life-threatening hyperkalemia tends to occur. Respiratory support may be required acutely for sudden deterioration in spontaneous ventilation secondary to muscle paralysis, as with our first patient. Hence, the early management of such patients in intensive care units, with external monitoring, is important. two
has
References
acute
«8).9
Segarl in 1959 reported a mortality rate in myoglobinuria of approximately 30 per cent, caused usually by acute renal failure or respiratory paralysis. 13,14 Since that time, the
1.
Segar,
W. E.:
Idiopathic paroxysmal myoglobinuria.
Pediatrics 23: 12, 1959. 2. Savage, D. C. L., Forbes, M., and Pearce, G. W.: Idiopathic rhabdomyolysis. Arch. Dis. Child.
594,1971. 46:
Wagner, H., and Glauser, E. M.: rapid simple accurate test for differentiating hemoglobinuria from myoglobinuria. Am. J.
3. Glauser, S. C., A
Med. Sci. 264: 135, 1972.
65
Downloaded from cpj.sagepub.com at UCSF LIBRARY & CKM on March 22, 2015
4.
Kagen, L.J.: Myoglobinuria syndromes. Am. J. Med.
264: Sci. 141, 1972. 5. Farar, B. E., Vawter, G. F., Wagner, R., Kery, S., and Porter, E. G.: Familial paroxysmal rhabdo42 : 196, 1967. myolysis in children. Am. J. Med. 6. Korein, J., Coggon, D. R., and Mowrey, F. H.: The clinical syndrome of paroxysmal paralytic myoof two cases and an analytic review of the literature. Neurology 9: 767, 1959.
globinuria. Report
7. Minow, R. A., Sherwood, G., Johnson, B. L., Jr., and Dornfeld, L.: Myoglobinuria associated with influenza A infection. Ann. Int. Med. 80:
359, 1974. 8.
L.: Myoglobinuria and renal failure associated with influenza. Ann. Intern. Med. 80:
Morgensen, J. 362, 1974.
9. Grossman, R. A., Hamilton, R. W., Morse, B. M., Penn, A. S., and Goldberg, M.: Rhabdomyolysis
and
acute
Ampicillin-Resistant Haemophilus Influenzae
a
and, specifically, meningitis caused strains is unknown. However, the consequences of ineffective or delayed proper treatment are such that primary therapy for patients with confirmed or suspected infection caused by ~I. influenzae should include chloramphenicol. Because of the rare but serious problem of irreversible aplastic anemia following the use of this drug, it should be used only for dear indications such as the above.
by ampicillin-resistant
°
The inclusion
February
May 1975,
Engl. J.
Med. 291:
Goldberg, M.: Acute tubular necrosis caused by exercise-induced myoglobinuria. Ann. Intern. Med. 77: 77, 1972. 11. Rowland, L. P., and Penn, A. S.: Myoglobinuria. Med. Clin. North Am. 56: 1233, 1972. 12. Rowland, L. P., Dunne, P. B., Penn, A. S., and Maher, J.: Myoglobinuria and muscular dystrophy. Arch. Neurol. 18: 141, 1968. 13. Borman, J. B., Davidson, J. T., and Bloudheim, S. H.: Idiopathic rhabdomolysis (myoglobinuria) as an acute respiratory problem. Br. Med. J. 2: 726, 1963. 14. Berenson, M., Yazvote, P., and Grace, W. J.: Idiopathic myoglobinuria with respiratory paralysis. Am. Rev. Resp. Dis. 94: 956, 1966.
1974 through total of 58 ampicillinresistant strains of Haemophilus influenzas have been submitted to the Antimicrobics Investigations Section of the CDC. Each strain was recovered from the blood or cerebrospinal fluid (CSF) of a childall less than five years old, all but three less than four years old. Meningitis was the most common manifestation of disease, occurring in 41 patients (71%). The outcome of illness was reported for 29 children with meningitis or bacteremia ; four (14%) died. These strains came from all regions of the United States. The proportion of H. influenza disease From
renal failure. N.
807, 1974. 10. Hamilton, R. W., Gardner, L. B., Penn, A. S., and
or
exclusion of H.
influenzae as the etiology of bacterial meningitis in young children can be expedited by the rapid perform-
ance of the gram stain and Quellung reaction with type B antiserum on CSF. In some hospitals counterimmunoelectrophoresis of blood or CSF may also serve to quickly establish the diagnosis.
of ampicillinof H. influenzae recovered from cases is important for clinicians who may wish to discontinue therapy with chloramphenicol and use ampicillin exclusively if results indicate that this will be successful. An
assessment
sensitivity
Tests for beta lactamase production can be performed as soon as growth of ~. influenzae is evident
agar. This provides a rapid method for screening for ampicillin-resistance, but if this test is on
negative, sensitivity
to
ampicillin
should be established by standard disk or tube dilution methods before chloramphenicol is dropped from therapy.-From CDC Morbidity and Mortality Weekly Report,~une 14, 1975.
66
Downloaded from cpj.sagepub.com at UCSF LIBRARY & CKM on March 22, 2015
’
Myoglobinuria The
Importance of Intensive Care and Peritoneal Dialysis
Elfrid
ACUTE
with Acute Renal Failure in Children
Cifuentes, M.D., Michael E. Norman, M.D., M. William Schwartz, M.D., Bruce Maley, LCDR, MC, USN, William Bason, CAPT, MC, USN
NECROSIS of muscle
lead disturbelectrolyte myoglobinuria, ances, acute renal failure, and even death. Early diagnosis and early treatment are of the utmost importance for a satisfactory recovery. There have been few reports of myoglobinuria with acute renal failure in the pediatric l~iterature.1-2 We here describe two children who illustrate the fulminant and lifethreatening potentialities of this syndrome, and the reversibility of acute renal failure with early peritoneal dialysis. to
can
severe
Case Reports Case 1 An eight-year-old black girl was transferred the US Naval Hospital of Philadelphia in February 1974. Her illness began four days prior to admission, with symptoms of an upper respiratory tract infection (cough and rhinitis), followed
to
From The Children’s
Hospital of Philadelphia and Department of Pediatrics, US Naval Hospital, Philadelphia, Pa. Correspondence to Michael E. Norman, M.D., The Children’s Hospital of Philadelphia, 34th Street and Civic Center Boulevard, Philadelphia, Pa. 19104. the
The views expressed herein are those of the authors and are not to be construed as official or as reflecting the views of the United States Navy or the Department of Defense.
severe bilateral anterior thigh pain. She had history of fever, nausea or vomiting, exposure to drugs, or chemicals. On admission to another hospital, physical and laboratory examinations were unrevealing except for a hematocrit of 46
by
no
Her urine was dark yellow with 4+ moderate glucose, a strongly positive o-toluidine test for occult blood, and one or two red blood cells per high power field but no casts. Over the next two and one-half days, anorexia, vomiting, lethargy, and somnolence were progressive. She exhibited delusional behavior. Urine output decreased and the color turned dark brown. Physical examination on transfer revealed a comatose child, with no auscultable or palpable blood pressure. She had Kussmaul-type respirations, with peripheral cyanosis and dilated pupils, and no spontaneous movements. The muscles were diffusely edematous. Laboratory reports were as follows: serum sodium 122 mEq/1, potassium 9.0 mEq/1, chloride 70 mEq/1, C02 18 mM/I; BUN 36 mg/dl; creatinine 3.4 mg/dl; calcium 7.2 mg/dl; phosphorus 11.3 mg/dl; lactic dehydrogenase 2,282 LU.lml, and creatinine phosphokinase 8,820 l.U./ml. Cultures of blood, urine, stool, and cerebrospinal fluid (CSF) were all negative. An EKG showed changes compatible with marked hyperkalemia. The urine was positive for myoglobin by spectrophotometry (600 and 800 m>)3 and by a hemagglutination inhibition test.**
per
cent.
protein,
*
Niyotel,
Ames
Company, Elkhart,
Ind.
63
Downloaded from cpj.sagepub.com at UCSF LIBRARY & CKM on March 22, 2015
The patient responded to treatment for shock and hyperkalemia, but a tracheostomy with artificial ventilation was needed for respiratory paralysis. Peritoneal dialysis was required because of azotemia and fluid overload from total anuria; this lasted for seven days. Diuresis commenced on the 14th hospital day. At the time of discharge, physical examination, muscle enzyme levels, and renal function were within normal limits.
associated with extreme muscular exertion. 1,2,4 A relationship to antecedent viral (e.g., gastrointestinal, respiratory) infections has been suggested but remains un-
Case 2
primary myopathy, seizures, drug overdose, or unusual exertion to explain muscle necrosis. A muscle biopsy in Case 2 revealed no virus-like particles, giant cells, or inclusion
proven. 2,6-8 In our two patients, rhabdomyolysis developed after upper respiratory tract infections, and progressed rapidly to anuric renal failure. Neither had evidence of trauma,
black girl was brought to The Hospital of Philadelphia with a sevenday history of upper respiratory tract infection, fever, vomiting, and progressive muscle pain A
13-year-old
Children’s
and weakness. She
was
in
acute
distress with
thready peripheral pulse (140/min)
bodies. The striking feature of our two cases was the complete anuria lasting one week, a distinctly unusual occurence in children with acute parenchymal renal failure from any cause. The alternative diagnosis of bilateral
a
and weak
respiratory effort (28/min). Blood pressure readings were unobtainable. Temperature was 38 C. She had diaphoresis and muscle tenderness and weakness over the thighs and lower extremities. Blood hemoglobin was 15.1 gznldl, hematocrit 42.9 per cent, leukocyte count 33,900/mm3, with 95 per cent neutrophils, and 5 per cent lymphocytes ; serum sodium 124 mEq/1, potassium 7.7 mEq/1, chloride 84 mEq/1, C02 11 mMll; BUN 39 mg/dl, creatinine 10.0 mg/dl; phosphorus 10.2 mgldl, calcium 5.0 mg/dl, glucose 180 mg/dl; SGOT 1,850 I.U./ml, SGPT 620 I.U./ml, lactic dehydrogenase 45,200 1. U./ml, and creatinine phosphokinase 100,000 to 269,000 l.U./ml. CSF and blood cultures were negative. treated with intravenous albumin, fluids, and hydrocortisone. No urine was passed after hydration and a single intravenous dose of mannitol. Bladder catheterization produced a few milliliters of dark brown urine; specific gravity was 1.025, protein 3+, glucose 2+, occult blood 3+ without red blood cells, and 3 to 5 white blood cells per high power field. No casts were seen, but the ammonium sulfate precipitation and hemagglutination inhibition tests (Myotel) were positive for myoglobin. Intermittent peritoneal dialysis was carried out for one week because of azotemia, hyperkalemia, and fluid overload secondary to complete anuria. Diuresis commenced on the eighth hospital day. Percutaneous renal biopsy revealed acute tubular necrosis with myoglobin casts. Biopsy of the left quadriceps muscle 15 weeks after the acute illness revealed nonspecific changes; no virus-like particles, giant cells, or inclusion bodies were seen. An ischemic exercise test was normal, with a threefold rise in venous lactate after one minute of ischemia. The patient made a full recovery.
She
Prompt institution of peritoneal dialysis is important because it is in the first three to five days that life-threatening hyperkalemia tends to occur.
was
Discussion
Myoglobinuria with acute renal failure is infrequent in childhood and is usually un-
.
renal cortical necrosis was considered with both children, since each presented to the hospital in shock, but their subsequent full recoveries made this diagnosis unlikely. A rental biopsy in Case 2 demonstrated acute tubular necrosis with myoglobin casts, hence it must be assumed that anuria resulted from the renal toxicity of heme pigment. Grossman, et al. have recently reviewed the theories to explain renal failure in heme pigmenturia.9 These include: 1) tubular plugging with myoglobin casts, 2) a primary decrease in glomular filtration rate, 3) direct nephrotoxicity with back diffusion into the circulation through damaged tubular epithelium, and 4) shunting of blood away from the cortex, with decreased glomular filtration. None of these theories alone seems to sufficiently explain the acute renal failure. Well-documented cases of acute tubular necrosis after exercise-induced myoglobinuria are rare.10 Nontraumatic rhabdomyolysis as the cause was 5 per cent in a large series of adults with acute renal failure reported by Grossman, et at.99
64
Downloaded from cpj.sagepub.com at UCSF LIBRARY & CKM on March 22, 2015
The
causes
globinuria globinuria
are
of myoglobinemia and myodiverse (Table 1). When myo-
is recurrent, a primary myopathy should be searched for. Because of the differences in protein binding and renal clearance, in myoglobinuria unlike hemoglobinuria the plasma may be normally colored. Mechanisms underlying myoglobinuria have recently been reviewed by Rowland and Penn. 11 Idiopathic rhabdomyolysis with myoglobinuria must be suspected whenever a child with fever, muscle pain, tenderness, weakness, and edema passes red or brown urine which gives a positive test for occult blood. Red blood cells of course are absent from the urine. Myoglobin may be differentiated from hemoglobin by a variety of techniques.~4 Spectrophotometry, readily available in most clinical laboratories, has traditionally been the standard method of identification. Technical problems, however, limit its usefulness. More sensitive techniques are immunologic in nature, and include polyacrylamide gel electrophoresis, immunodiffusion, 10.12 and the specific hemagglutination inhibition assay used with our patients. Pigmented granular casts do not differentiate myoglobinuria from hemoglobinuria (in the very small quantities of urine passed by our patients,
pigmented granular
casts were not
seen).
Necrosis of striated or cardiac muscle is reflected in elevation of muscle enzyme levels in serum. Serum glutamic oxaloacetic trans-
aminase, serum glutamic pyruvic transaminase, creatinine phosphokinase, and lactic
dehydrogenase were all strikingly elevated in patients. In addition, leakage of intracellular muscle constituents (e.,~., creatinine, potassium, phosphorus) into the circulation produces characteristic and striking elevations of serum levels of creatinine, potassium, and phosphate. Hypocalcemia often appears. An important additional clue to the diagnosis our
when
renal failure occurs is the disproportionate rise in serum creatinine and resultant lowered BUN: creatinine ratio
TABLE 1. Causes
of Myoglobinemia and Myoglobinuria
management of these
complications dramatically improved. Both of our patients recovered completely despite initial shock followed by complete anuria. Prompt institution of peritoneal dialysis is important because it is in the first three to five days, that life-threatening hyperkalemia tends to occur. Respiratory support may be required acutely for sudden deterioration in spontaneous ventilation secondary to muscle paralysis, as with our first patient. Hence, the early management of such patients in intensive care units, with external monitoring, is important. two
has
References
acute
«8).9
Segarl in 1959 reported a mortality rate in myoglobinuria of approximately 30 per cent, caused usually by acute renal failure or respiratory paralysis. 13,14 Since that time, the
1.
Segar,
W. E.:
Idiopathic paroxysmal myoglobinuria.
Pediatrics 23: 12, 1959. 2. Savage, D. C. L., Forbes, M., and Pearce, G. W.: Idiopathic rhabdomyolysis. Arch. Dis. Child.
594,1971. 46:
Wagner, H., and Glauser, E. M.: rapid simple accurate test for differentiating hemoglobinuria from myoglobinuria. Am. J.
3. Glauser, S. C., A
Med. Sci. 264: 135, 1972.
65
Downloaded from cpj.sagepub.com at UCSF LIBRARY & CKM on March 22, 2015
4.
Kagen, L.J.: Myoglobinuria syndromes. Am. J. Med.
264: Sci. 141, 1972. 5. Farar, B. E., Vawter, G. F., Wagner, R., Kery, S., and Porter, E. G.: Familial paroxysmal rhabdo42 : 196, 1967. myolysis in children. Am. J. Med. 6. Korein, J., Coggon, D. R., and Mowrey, F. H.: The clinical syndrome of paroxysmal paralytic myoof two cases and an analytic review of the literature. Neurology 9: 767, 1959.
globinuria. Report
7. Minow, R. A., Sherwood, G., Johnson, B. L., Jr., and Dornfeld, L.: Myoglobinuria associated with influenza A infection. Ann. Int. Med. 80:
359, 1974. 8.
L.: Myoglobinuria and renal failure associated with influenza. Ann. Intern. Med. 80:
Morgensen, J. 362, 1974.
9. Grossman, R. A., Hamilton, R. W., Morse, B. M., Penn, A. S., and Goldberg, M.: Rhabdomyolysis
and
acute
Ampicillin-Resistant Haemophilus Influenzae
a
and, specifically, meningitis caused strains is unknown. However, the consequences of ineffective or delayed proper treatment are such that primary therapy for patients with confirmed or suspected infection caused by ~I. influenzae should include chloramphenicol. Because of the rare but serious problem of irreversible aplastic anemia following the use of this drug, it should be used only for dear indications such as the above.
by ampicillin-resistant
°
The inclusion
February
May 1975,
Engl. J.
Med. 291:
Goldberg, M.: Acute tubular necrosis caused by exercise-induced myoglobinuria. Ann. Intern. Med. 77: 77, 1972. 11. Rowland, L. P., and Penn, A. S.: Myoglobinuria. Med. Clin. North Am. 56: 1233, 1972. 12. Rowland, L. P., Dunne, P. B., Penn, A. S., and Maher, J.: Myoglobinuria and muscular dystrophy. Arch. Neurol. 18: 141, 1968. 13. Borman, J. B., Davidson, J. T., and Bloudheim, S. H.: Idiopathic rhabdomolysis (myoglobinuria) as an acute respiratory problem. Br. Med. J. 2: 726, 1963. 14. Berenson, M., Yazvote, P., and Grace, W. J.: Idiopathic myoglobinuria with respiratory paralysis. Am. Rev. Resp. Dis. 94: 956, 1966.
1974 through total of 58 ampicillinresistant strains of Haemophilus influenzas have been submitted to the Antimicrobics Investigations Section of the CDC. Each strain was recovered from the blood or cerebrospinal fluid (CSF) of a childall less than five years old, all but three less than four years old. Meningitis was the most common manifestation of disease, occurring in 41 patients (71%). The outcome of illness was reported for 29 children with meningitis or bacteremia ; four (14%) died. These strains came from all regions of the United States. The proportion of H. influenza disease From
renal failure. N.
807, 1974. 10. Hamilton, R. W., Gardner, L. B., Penn, A. S., and
or
exclusion of H.
influenzae as the etiology of bacterial meningitis in young children can be expedited by the rapid perform-
ance of the gram stain and Quellung reaction with type B antiserum on CSF. In some hospitals counterimmunoelectrophoresis of blood or CSF may also serve to quickly establish the diagnosis.
of ampicillinof H. influenzae recovered from cases is important for clinicians who may wish to discontinue therapy with chloramphenicol and use ampicillin exclusively if results indicate that this will be successful. An
assessment
sensitivity
Tests for beta lactamase production can be performed as soon as growth of ~. influenzae is evident
agar. This provides a rapid method for screening for ampicillin-resistance, but if this test is on
negative, sensitivity
to
ampicillin
should be established by standard disk or tube dilution methods before chloramphenicol is dropped from therapy.-From CDC Morbidity and Mortality Weekly Report,~une 14, 1975.
66
Downloaded from cpj.sagepub.com at UCSF LIBRARY & CKM on March 22, 2015
’
