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The Prognostic Value of Hyponatremia
Race, Ethnicity, and Perception of Prostate Cancer Risk
Grand Rounds: Woman, 39, With Leg Weakness After Exercise Class
A 39-year-old woman presented to the emergency department (ED) with a chief complaint of muscle aches and pain. She stated that three days earlier, she had begun exercising in a 45-minute “spinning” class (ie, riding a stationary bicycle with a weighted front wheel). The patient had not engaged in any aerobic exercise for at least six months before the spinning class. She mentioned that much older participants in the class were outperforming her, but she did not feel the need to keep up with them.
After dismounting, the woman said, she experienced weakness in her legs and had great difficulty ambulating. She went home, took 400 mg of ibuprofen, and went to bed. She awoke with pain and swelling in both thighs and continued to take ibuprofen, in addition to applying a topical mentholated preparation to her thighs. She took an Epsom salts bath two days later.
On the morning of the third day after the spinning class, she voided black urine and presented to the ED.
The patient had no significant medical history. Surgical history was limited to removal of a ganglion cyst on her wrist. She denied any history of seizure disorder, thyroid disease, hepatitis, heart disease, or hyperlipidemia.
The patient had been taking ibuprofen as needed since the spinning class. She was taking no other medications. She denied any allergies to drugs or food.
The patient admitted to smoking one pack of cigarettes per week and to occasional alcohol consumption but denied use of illicit drugs. She was employed as an executive officer for a large business association.
On physical examination, the patient’s vital signs were blood pressure, 134/73 mm/Hg; pulse, 86 beats/min; and respirations, 16 breaths/min. She was afebrile, alert, and oriented. Her sclera were nonicteric. Her neck was supple with no anterior cervical lymphadenopathy. There was no thyroid enlargement, her lungs were clear to auscultation, and her heart sounds were regular. There was no peripheral edema, and dorsalis pedis pulses were present bilaterally. Her thighs appeared swollen but were not tender to palpation.
The patient’s history, combined with an extremely high level of serum creatine phosphokinase (CPK; ie, 123,800 U/L [reference range, 45 to 260 U/L1]), confirmed a diagnosis of rhabdomyolysis. She was admitted for close observation. The patient’s urinalysis revealed 2 to 5 red blood cells and 6 to 10 white blood cells per high-power field. Moderate occult blood was detected, with no casts or protein noted. A urine myoglobin test was not performed.
The patient underwent IV hydration with dextrose 5% in water and three ampules of sodium bicarbonate after being given a 2.0-L saline bolus. Ibuprofen was discontinued. IV hydration with bicarbonate solution was continued until the patient’s CPK level declined significantly. She underwent daily laboratory testing (see Table 1). Her renal function remained stable, and she was discharged on hospital day 7.
DISCUSSION
Rhabdomyolysis is a clinical condition defined as muscle necrosis resulting from the release of intracellular skeletal muscle components (including myoglobin, CPK, potassium, phosphorus, and aldolase) into the extracellular compartment.1-3 The condition was first described during the bombing of London in World War II, with high incidence of crush injuries, shock, and associated kidney damage.4 The preponderance of such injuries during a 1988 earthquake in Armenia led the International Society of Nephrology to form its Renal Disaster Relief Task Force, which has provided support at numerous other disaster scenes since then.5
Rhabdomyolysis has been identified with a variety of pathologic events: those that cause muscle trauma, those associated with muscle use or overuse, and other etiologies involving genetic, metabolic, infectious, or pharmaceutical factors.1 Many of the reported causes of rhabdomyolysis are listed in Table 2.1,2
For patients with muscle trauma, the etiology of rhabdomyolysis is clear, but for those with other disease states, diagnosis may be more elusive. Patients who present with rhabdomyolysis after excessive exercise, for example, may have underlying metabolic disorders that predispose them to exertional rhabdomyolysis, such as chronic hypokalemia resulting from primary hyperaldosteronism.1 Others may have a muscle enzyme deficiency, as in McArdle’s syndrome or carnitine deficiency.6
Alterations in blood chemistries can also contribute to development of rhabdomyolysis, even when more obvious etiologies for muscle necrosis are evident. Hypokalemia interferes with the vasodilation that normally occurs during exercise to increase muscle blood flow.1,7,8 Continued exercise can lead to muscle necrosis, raising a concern for athletes who take diuretics.1 Hypophosphatemia leads to a state of muscle necrosis; this is of particular concern for alcoholic patients who receive hyperalimentation without repletion of phosphates.9
Diagnosis
Patients with rhabdomyolysis usually present with myalgias, darkened urine (red, brown, or black), and a clinical scenario that corroborates the diagnosis (ie, history of trauma, excessive exercise, use of an offending medication).1 Some patients may have minimal to absent symptoms or symptoms that occur only after exercise.3
A careful history is key. While traumatic causes are obvious, it is important to ask a patient with rhabdomyolysis after exertion about previous history of excessive weakness during or immediately after exercise, excessive cramping, or discoloration of urine after exercise. The family history may point to a genetic abnormality. A thorough understanding of the patient’s use of medications, including OTC agents, is also important. Rhabdomyolysis has been reported in patients who use herbal remedies, including those taken to facilitate weight loss or to improve lipid profiles.10,11
For patients suspected of having rhabdomyolysis, a serum CPK level should be obtained; results exceeding normal values by five times confirm the diagnosis.3 Measurements for potassium, phosphorus, and calcium are also important to determine, as is renal function. A high level of serum aldolase (an enzyme that breaks down glucose in muscle tissue) can also support a diagnosis of rhabdomyolysis.1,12 Urinalysis and urine myoglobin testing are also warranted, although a negative urine myoglobin test result does not rule out rhabdomyolysis in the presence of an elevated CPK level. Myoglobin is cleared rapidly by the kidneys, whereas serum CPK levels change slowly.1
Any patient who presents with acute rhabdomyolysis and low to normal values for potassium or phosphate should be evaluated further for hypokalemia and hypophosphatemia as contributing or etiologic factors. Hypocalcemia may occur in the early course of rhabdomyolysis as calcium salt is deposited in muscle tissue. Patients recovering from rhabdomyolysis may experience rebound hypercalcemia as the damaged muscle releases the deposited calcium.7,13
In most cases of rhabdomyolysis, only laboratory values are needed to make the diagnosis and follow the course of the episode.1 However, when the etiology appears to involve metabolic deficiencies or genetic etiologies, it may become necessary to order additional diagnostic tests. These may include tests for thyroid function, a carnitine level to screen for glycogen storage diseases, and toxin screening (eg, for illicit drugs, such as cocaine).2,6
Treatment and Management
Effective treatment of rhabdomyolysis relies on recognizing the underlying disorder.1 For patients with muscle trauma (eg, crush injury) or muscle overuse, the mainstay of treatment is aggressive fluid resuscitation and prevention of acute injury to the kidneys.13 As for patients with an injury induced by a pharmaceutical agent or a toxin, removal of the offending agent is required, followed by hydration and prevention of renal damage. Supportive care during an infectious illness is also essential.14
Additionally, treatment must address the complications inherent with rhabdomyolysis.1 In addition to CPK, potassium, phosphorus, and myoglobin are also released from skeletal muscle tissue. Hyperkalemia can be fatal, and potassium levels must be monitored closely to avert this condition.7,8,13 During an episode of rhabdomyolysis, normal levels of both potassium and phosphorus should raise the clinician’s suspicion for underlying hypokalemia and hypophosphatemia—conditions that may have contributed to the episode of rhabdomyolysis. Hypocalcemia may also develop.13
Released myoglobin may cause acute kidney injury, as is the case in 33% to 50% of patients with rhabdomyolysis.3 In early studies, it was determined that alkalinizing the urine with IV isotonic bicarbonate might thwart onset of acute kidney injury.1,2,15 Time is critical, and even on the battlefield or at the scene of a recent disaster, most attempts at resuscitation are begun immediately. IV access may be problematic, but administration of oral bicarbonate solutions has also proven effective.15 Close follow-up of the serum urea and creatinine levels and measurement of the urine pH during alkalinization is warranted throughout the course of the episode.
Unfortunately, some patients respond poorly to these conservative measures, and the released myoglobin can cause renal tubular blockage and necrosis, resulting in acute kidney injury.1 Renal replacement therapy may be required.16 However, most episodes of dialysis-dependent acute renal injury do subside with time.
For patients with less elusive causes of rhabdomyolysis, treatment will hinge on a workup of the possible etiologies and follow-up treatment to target the apparent cause. For example, carnitine may be administered to patients with carnitine deficiency, and hypokalemic patients may be given potassium.1,6,7 These patients will also need counseling before they consider engaging in an exercise program.
Patient’s Outcome
The case patient presented with exertional rhabdomyolysis; improper hydration, severe deconditioning, and a relatively low serum potassium level may all have contributed to the muscle necrosis she experienced. She was given IV alkaline solutions and did not develop acute kidney injury. She was discharged from the hospital and at the time of this writing was awaiting outpatient follow-up.
It should be interesting to see whether the case patient experiences any further episodes of severe weakness after engaging in exercise. Her low-normal potassium level (reference range, 3.5 to 5.3 mmol/L17) warrants further follow-up, as does her mildly elevated thyroid-stimulating hormone level (reference range, 0.5 to 4.7 mcIU/mL17).
CONCLUSION
Patients with rhabdomyolysis may present with muscle aches, darkened urine, and/or weakness; an elevated CPK level confirms the diagnosis. Management is mainly conservative, with IV hydration accompanied by alkalinizing the urine and correcting any metabolic abnormalities, such as potassium deficiencies. For the few patients who experience severe acute kidney injury, renal replacement therapy may be necessary.
While most causes of rhabdomyolysis have obvious clinical scenarios, such as a crush injury, a search for muscle enzyme deficiencies, disorders of potassium homeostasis, and thyroid abnormalities is also warranted in patients who present with exertional rhabdomyolysis.
1. Huerta-Alardín AL, Varon J, Marik PE. Bench-to-bedside review: rhabdomyolysis—an overview for clinicians. Crit Care. 2005;9(2):158-169.
2. Warren JD, Blumbergs PC, Thompson PD. Rhabdomyolysis: a review. Muscle Nerve. 2002;25(3):332-347.
3. Lima RSA, da Silva GB Jr, Liborio AB, Daher ED. Acute kidney injury due to rhabdomyolysis. Saudi J Kidney Dis Transpl. 2008;19(5):721-729.
4. Bywaters EG, Beall D. Crush injuries with impairment of renal function [reprinted from BMJ, 1941]. J Am Soc Nephrol. 1998;9(2):322-332.
5. Vanholder R, Van Biesen W, Lameire N, Sever MS; International Society of Nephrology/Renal Disaster Relief Task Force. The role of the International Society of Nephrology/Renal Disaster Relief Task Force in the rescue of renal disaster victims. Contrib Nephrol. 2007;156:325-332.
6. Toledo R, López V, Martín G, et al. Rhabdomyolysis due to enzyme deficiency in muscles. Nefrología. 2009;29(1):77-80.
7. Agrawal S, Agrawal V, Taneja A. Hypokalemia causing rhabdomyolysis resulting in life-threatening hyperkalemia. Pediatr Nephrol. 2006;221(2): 289-291.
8. Knochel JP, Schlein EM. On the mechanism of rhabdomyolysis in potassium depletion. J Clin Invest. 1972:51(7):1750-1758.
9. Knochel JP. Hypophosphatemia and rhabdomyolysis. Am J Med. 1992;92(5):455-457.
10. Mansi IA, Huang J. Rhabdomyolysis in response to weight-loss herbal medicine. Am J Med Sci. 2004; 327(6): 356-357.
11. Heber D, Yip I, Ashley JM, et al. Cholesterol-lowering effects of a proprietary Chinese red-yeast-rice dietary supplement. Am J Clin Nutr. 1999;69(2): 231-236.
12. Hooda AK, Narula AS. Exertional rhabdomyolysis causing acute renal failure. Med J Armed Forces India. 2005;61(4):395-396.
13. Chatzizisis YS, Misirli G, Hatzitolios AI, Giannoglou GD. The syndrome of rhabdomyolysis: complications and treatment. Eur J Intern Med. 2008;19(8): 568-574.
14. Blanco JR, Zabalza M, Salcedo J, et al. Rhabdomyolysis of infectious and noninfectious causes. South Med J. 2002;95(5):542-544.
15. Ron D, Taitelman U, Michaelson M, et al. Prevention of acute renal failure in traumatic rhabdomyolysis. Arch Intern Med. 1984;144(2):277-280.
16. Soni SS, Nagarik AP, Adikey GK, Raman A. Using continuous renal replacement therapy to manage patients of shock and acute renal failure. J Emerg Trauma Shock. 2009;2(1):19-22.
17. Normal laboratory values. In: Beers MH, Berkow R, eds. The Merck Manual of Diagnosis and Therapy. 17th ed. Whitehouse Station, NJ: Merck Research Laboratories; 1999:2526-2546.
A 39-year-old woman presented to the emergency department (ED) with a chief complaint of muscle aches and pain. She stated that three days earlier, she had begun exercising in a 45-minute “spinning” class (ie, riding a stationary bicycle with a weighted front wheel). The patient had not engaged in any aerobic exercise for at least six months before the spinning class. She mentioned that much older participants in the class were outperforming her, but she did not feel the need to keep up with them.
After dismounting, the woman said, she experienced weakness in her legs and had great difficulty ambulating. She went home, took 400 mg of ibuprofen, and went to bed. She awoke with pain and swelling in both thighs and continued to take ibuprofen, in addition to applying a topical mentholated preparation to her thighs. She took an Epsom salts bath two days later.
On the morning of the third day after the spinning class, she voided black urine and presented to the ED.
The patient had no significant medical history. Surgical history was limited to removal of a ganglion cyst on her wrist. She denied any history of seizure disorder, thyroid disease, hepatitis, heart disease, or hyperlipidemia.
The patient had been taking ibuprofen as needed since the spinning class. She was taking no other medications. She denied any allergies to drugs or food.
The patient admitted to smoking one pack of cigarettes per week and to occasional alcohol consumption but denied use of illicit drugs. She was employed as an executive officer for a large business association.
On physical examination, the patient’s vital signs were blood pressure, 134/73 mm/Hg; pulse, 86 beats/min; and respirations, 16 breaths/min. She was afebrile, alert, and oriented. Her sclera were nonicteric. Her neck was supple with no anterior cervical lymphadenopathy. There was no thyroid enlargement, her lungs were clear to auscultation, and her heart sounds were regular. There was no peripheral edema, and dorsalis pedis pulses were present bilaterally. Her thighs appeared swollen but were not tender to palpation.
The patient’s history, combined with an extremely high level of serum creatine phosphokinase (CPK; ie, 123,800 U/L [reference range, 45 to 260 U/L1]), confirmed a diagnosis of rhabdomyolysis. She was admitted for close observation. The patient’s urinalysis revealed 2 to 5 red blood cells and 6 to 10 white blood cells per high-power field. Moderate occult blood was detected, with no casts or protein noted. A urine myoglobin test was not performed.
The patient underwent IV hydration with dextrose 5% in water and three ampules of sodium bicarbonate after being given a 2.0-L saline bolus. Ibuprofen was discontinued. IV hydration with bicarbonate solution was continued until the patient’s CPK level declined significantly. She underwent daily laboratory testing (see Table 1). Her renal function remained stable, and she was discharged on hospital day 7.
DISCUSSION
Rhabdomyolysis is a clinical condition defined as muscle necrosis resulting from the release of intracellular skeletal muscle components (including myoglobin, CPK, potassium, phosphorus, and aldolase) into the extracellular compartment.1-3 The condition was first described during the bombing of London in World War II, with high incidence of crush injuries, shock, and associated kidney damage.4 The preponderance of such injuries during a 1988 earthquake in Armenia led the International Society of Nephrology to form its Renal Disaster Relief Task Force, which has provided support at numerous other disaster scenes since then.5
Rhabdomyolysis has been identified with a variety of pathologic events: those that cause muscle trauma, those associated with muscle use or overuse, and other etiologies involving genetic, metabolic, infectious, or pharmaceutical factors.1 Many of the reported causes of rhabdomyolysis are listed in Table 2.1,2
For patients with muscle trauma, the etiology of rhabdomyolysis is clear, but for those with other disease states, diagnosis may be more elusive. Patients who present with rhabdomyolysis after excessive exercise, for example, may have underlying metabolic disorders that predispose them to exertional rhabdomyolysis, such as chronic hypokalemia resulting from primary hyperaldosteronism.1 Others may have a muscle enzyme deficiency, as in McArdle’s syndrome or carnitine deficiency.6
Alterations in blood chemistries can also contribute to development of rhabdomyolysis, even when more obvious etiologies for muscle necrosis are evident. Hypokalemia interferes with the vasodilation that normally occurs during exercise to increase muscle blood flow.1,7,8 Continued exercise can lead to muscle necrosis, raising a concern for athletes who take diuretics.1 Hypophosphatemia leads to a state of muscle necrosis; this is of particular concern for alcoholic patients who receive hyperalimentation without repletion of phosphates.9
Diagnosis
Patients with rhabdomyolysis usually present with myalgias, darkened urine (red, brown, or black), and a clinical scenario that corroborates the diagnosis (ie, history of trauma, excessive exercise, use of an offending medication).1 Some patients may have minimal to absent symptoms or symptoms that occur only after exercise.3
A careful history is key. While traumatic causes are obvious, it is important to ask a patient with rhabdomyolysis after exertion about previous history of excessive weakness during or immediately after exercise, excessive cramping, or discoloration of urine after exercise. The family history may point to a genetic abnormality. A thorough understanding of the patient’s use of medications, including OTC agents, is also important. Rhabdomyolysis has been reported in patients who use herbal remedies, including those taken to facilitate weight loss or to improve lipid profiles.10,11
For patients suspected of having rhabdomyolysis, a serum CPK level should be obtained; results exceeding normal values by five times confirm the diagnosis.3 Measurements for potassium, phosphorus, and calcium are also important to determine, as is renal function. A high level of serum aldolase (an enzyme that breaks down glucose in muscle tissue) can also support a diagnosis of rhabdomyolysis.1,12 Urinalysis and urine myoglobin testing are also warranted, although a negative urine myoglobin test result does not rule out rhabdomyolysis in the presence of an elevated CPK level. Myoglobin is cleared rapidly by the kidneys, whereas serum CPK levels change slowly.1
Any patient who presents with acute rhabdomyolysis and low to normal values for potassium or phosphate should be evaluated further for hypokalemia and hypophosphatemia as contributing or etiologic factors. Hypocalcemia may occur in the early course of rhabdomyolysis as calcium salt is deposited in muscle tissue. Patients recovering from rhabdomyolysis may experience rebound hypercalcemia as the damaged muscle releases the deposited calcium.7,13
In most cases of rhabdomyolysis, only laboratory values are needed to make the diagnosis and follow the course of the episode.1 However, when the etiology appears to involve metabolic deficiencies or genetic etiologies, it may become necessary to order additional diagnostic tests. These may include tests for thyroid function, a carnitine level to screen for glycogen storage diseases, and toxin screening (eg, for illicit drugs, such as cocaine).2,6
Treatment and Management
Effective treatment of rhabdomyolysis relies on recognizing the underlying disorder.1 For patients with muscle trauma (eg, crush injury) or muscle overuse, the mainstay of treatment is aggressive fluid resuscitation and prevention of acute injury to the kidneys.13 As for patients with an injury induced by a pharmaceutical agent or a toxin, removal of the offending agent is required, followed by hydration and prevention of renal damage. Supportive care during an infectious illness is also essential.14
Additionally, treatment must address the complications inherent with rhabdomyolysis.1 In addition to CPK, potassium, phosphorus, and myoglobin are also released from skeletal muscle tissue. Hyperkalemia can be fatal, and potassium levels must be monitored closely to avert this condition.7,8,13 During an episode of rhabdomyolysis, normal levels of both potassium and phosphorus should raise the clinician’s suspicion for underlying hypokalemia and hypophosphatemia—conditions that may have contributed to the episode of rhabdomyolysis. Hypocalcemia may also develop.13
Released myoglobin may cause acute kidney injury, as is the case in 33% to 50% of patients with rhabdomyolysis.3 In early studies, it was determined that alkalinizing the urine with IV isotonic bicarbonate might thwart onset of acute kidney injury.1,2,15 Time is critical, and even on the battlefield or at the scene of a recent disaster, most attempts at resuscitation are begun immediately. IV access may be problematic, but administration of oral bicarbonate solutions has also proven effective.15 Close follow-up of the serum urea and creatinine levels and measurement of the urine pH during alkalinization is warranted throughout the course of the episode.
Unfortunately, some patients respond poorly to these conservative measures, and the released myoglobin can cause renal tubular blockage and necrosis, resulting in acute kidney injury.1 Renal replacement therapy may be required.16 However, most episodes of dialysis-dependent acute renal injury do subside with time.
For patients with less elusive causes of rhabdomyolysis, treatment will hinge on a workup of the possible etiologies and follow-up treatment to target the apparent cause. For example, carnitine may be administered to patients with carnitine deficiency, and hypokalemic patients may be given potassium.1,6,7 These patients will also need counseling before they consider engaging in an exercise program.
Patient’s Outcome
The case patient presented with exertional rhabdomyolysis; improper hydration, severe deconditioning, and a relatively low serum potassium level may all have contributed to the muscle necrosis she experienced. She was given IV alkaline solutions and did not develop acute kidney injury. She was discharged from the hospital and at the time of this writing was awaiting outpatient follow-up.
It should be interesting to see whether the case patient experiences any further episodes of severe weakness after engaging in exercise. Her low-normal potassium level (reference range, 3.5 to 5.3 mmol/L17) warrants further follow-up, as does her mildly elevated thyroid-stimulating hormone level (reference range, 0.5 to 4.7 mcIU/mL17).
CONCLUSION
Patients with rhabdomyolysis may present with muscle aches, darkened urine, and/or weakness; an elevated CPK level confirms the diagnosis. Management is mainly conservative, with IV hydration accompanied by alkalinizing the urine and correcting any metabolic abnormalities, such as potassium deficiencies. For the few patients who experience severe acute kidney injury, renal replacement therapy may be necessary.
While most causes of rhabdomyolysis have obvious clinical scenarios, such as a crush injury, a search for muscle enzyme deficiencies, disorders of potassium homeostasis, and thyroid abnormalities is also warranted in patients who present with exertional rhabdomyolysis.
A 39-year-old woman presented to the emergency department (ED) with a chief complaint of muscle aches and pain. She stated that three days earlier, she had begun exercising in a 45-minute “spinning” class (ie, riding a stationary bicycle with a weighted front wheel). The patient had not engaged in any aerobic exercise for at least six months before the spinning class. She mentioned that much older participants in the class were outperforming her, but she did not feel the need to keep up with them.
After dismounting, the woman said, she experienced weakness in her legs and had great difficulty ambulating. She went home, took 400 mg of ibuprofen, and went to bed. She awoke with pain and swelling in both thighs and continued to take ibuprofen, in addition to applying a topical mentholated preparation to her thighs. She took an Epsom salts bath two days later.
On the morning of the third day after the spinning class, she voided black urine and presented to the ED.
The patient had no significant medical history. Surgical history was limited to removal of a ganglion cyst on her wrist. She denied any history of seizure disorder, thyroid disease, hepatitis, heart disease, or hyperlipidemia.
The patient had been taking ibuprofen as needed since the spinning class. She was taking no other medications. She denied any allergies to drugs or food.
The patient admitted to smoking one pack of cigarettes per week and to occasional alcohol consumption but denied use of illicit drugs. She was employed as an executive officer for a large business association.
On physical examination, the patient’s vital signs were blood pressure, 134/73 mm/Hg; pulse, 86 beats/min; and respirations, 16 breaths/min. She was afebrile, alert, and oriented. Her sclera were nonicteric. Her neck was supple with no anterior cervical lymphadenopathy. There was no thyroid enlargement, her lungs were clear to auscultation, and her heart sounds were regular. There was no peripheral edema, and dorsalis pedis pulses were present bilaterally. Her thighs appeared swollen but were not tender to palpation.
The patient’s history, combined with an extremely high level of serum creatine phosphokinase (CPK; ie, 123,800 U/L [reference range, 45 to 260 U/L1]), confirmed a diagnosis of rhabdomyolysis. She was admitted for close observation. The patient’s urinalysis revealed 2 to 5 red blood cells and 6 to 10 white blood cells per high-power field. Moderate occult blood was detected, with no casts or protein noted. A urine myoglobin test was not performed.
The patient underwent IV hydration with dextrose 5% in water and three ampules of sodium bicarbonate after being given a 2.0-L saline bolus. Ibuprofen was discontinued. IV hydration with bicarbonate solution was continued until the patient’s CPK level declined significantly. She underwent daily laboratory testing (see Table 1). Her renal function remained stable, and she was discharged on hospital day 7.
DISCUSSION
Rhabdomyolysis is a clinical condition defined as muscle necrosis resulting from the release of intracellular skeletal muscle components (including myoglobin, CPK, potassium, phosphorus, and aldolase) into the extracellular compartment.1-3 The condition was first described during the bombing of London in World War II, with high incidence of crush injuries, shock, and associated kidney damage.4 The preponderance of such injuries during a 1988 earthquake in Armenia led the International Society of Nephrology to form its Renal Disaster Relief Task Force, which has provided support at numerous other disaster scenes since then.5
Rhabdomyolysis has been identified with a variety of pathologic events: those that cause muscle trauma, those associated with muscle use or overuse, and other etiologies involving genetic, metabolic, infectious, or pharmaceutical factors.1 Many of the reported causes of rhabdomyolysis are listed in Table 2.1,2
For patients with muscle trauma, the etiology of rhabdomyolysis is clear, but for those with other disease states, diagnosis may be more elusive. Patients who present with rhabdomyolysis after excessive exercise, for example, may have underlying metabolic disorders that predispose them to exertional rhabdomyolysis, such as chronic hypokalemia resulting from primary hyperaldosteronism.1 Others may have a muscle enzyme deficiency, as in McArdle’s syndrome or carnitine deficiency.6
Alterations in blood chemistries can also contribute to development of rhabdomyolysis, even when more obvious etiologies for muscle necrosis are evident. Hypokalemia interferes with the vasodilation that normally occurs during exercise to increase muscle blood flow.1,7,8 Continued exercise can lead to muscle necrosis, raising a concern for athletes who take diuretics.1 Hypophosphatemia leads to a state of muscle necrosis; this is of particular concern for alcoholic patients who receive hyperalimentation without repletion of phosphates.9
Diagnosis
Patients with rhabdomyolysis usually present with myalgias, darkened urine (red, brown, or black), and a clinical scenario that corroborates the diagnosis (ie, history of trauma, excessive exercise, use of an offending medication).1 Some patients may have minimal to absent symptoms or symptoms that occur only after exercise.3
A careful history is key. While traumatic causes are obvious, it is important to ask a patient with rhabdomyolysis after exertion about previous history of excessive weakness during or immediately after exercise, excessive cramping, or discoloration of urine after exercise. The family history may point to a genetic abnormality. A thorough understanding of the patient’s use of medications, including OTC agents, is also important. Rhabdomyolysis has been reported in patients who use herbal remedies, including those taken to facilitate weight loss or to improve lipid profiles.10,11
For patients suspected of having rhabdomyolysis, a serum CPK level should be obtained; results exceeding normal values by five times confirm the diagnosis.3 Measurements for potassium, phosphorus, and calcium are also important to determine, as is renal function. A high level of serum aldolase (an enzyme that breaks down glucose in muscle tissue) can also support a diagnosis of rhabdomyolysis.1,12 Urinalysis and urine myoglobin testing are also warranted, although a negative urine myoglobin test result does not rule out rhabdomyolysis in the presence of an elevated CPK level. Myoglobin is cleared rapidly by the kidneys, whereas serum CPK levels change slowly.1
Any patient who presents with acute rhabdomyolysis and low to normal values for potassium or phosphate should be evaluated further for hypokalemia and hypophosphatemia as contributing or etiologic factors. Hypocalcemia may occur in the early course of rhabdomyolysis as calcium salt is deposited in muscle tissue. Patients recovering from rhabdomyolysis may experience rebound hypercalcemia as the damaged muscle releases the deposited calcium.7,13
In most cases of rhabdomyolysis, only laboratory values are needed to make the diagnosis and follow the course of the episode.1 However, when the etiology appears to involve metabolic deficiencies or genetic etiologies, it may become necessary to order additional diagnostic tests. These may include tests for thyroid function, a carnitine level to screen for glycogen storage diseases, and toxin screening (eg, for illicit drugs, such as cocaine).2,6
Treatment and Management
Effective treatment of rhabdomyolysis relies on recognizing the underlying disorder.1 For patients with muscle trauma (eg, crush injury) or muscle overuse, the mainstay of treatment is aggressive fluid resuscitation and prevention of acute injury to the kidneys.13 As for patients with an injury induced by a pharmaceutical agent or a toxin, removal of the offending agent is required, followed by hydration and prevention of renal damage. Supportive care during an infectious illness is also essential.14
Additionally, treatment must address the complications inherent with rhabdomyolysis.1 In addition to CPK, potassium, phosphorus, and myoglobin are also released from skeletal muscle tissue. Hyperkalemia can be fatal, and potassium levels must be monitored closely to avert this condition.7,8,13 During an episode of rhabdomyolysis, normal levels of both potassium and phosphorus should raise the clinician’s suspicion for underlying hypokalemia and hypophosphatemia—conditions that may have contributed to the episode of rhabdomyolysis. Hypocalcemia may also develop.13
Released myoglobin may cause acute kidney injury, as is the case in 33% to 50% of patients with rhabdomyolysis.3 In early studies, it was determined that alkalinizing the urine with IV isotonic bicarbonate might thwart onset of acute kidney injury.1,2,15 Time is critical, and even on the battlefield or at the scene of a recent disaster, most attempts at resuscitation are begun immediately. IV access may be problematic, but administration of oral bicarbonate solutions has also proven effective.15 Close follow-up of the serum urea and creatinine levels and measurement of the urine pH during alkalinization is warranted throughout the course of the episode.
Unfortunately, some patients respond poorly to these conservative measures, and the released myoglobin can cause renal tubular blockage and necrosis, resulting in acute kidney injury.1 Renal replacement therapy may be required.16 However, most episodes of dialysis-dependent acute renal injury do subside with time.
For patients with less elusive causes of rhabdomyolysis, treatment will hinge on a workup of the possible etiologies and follow-up treatment to target the apparent cause. For example, carnitine may be administered to patients with carnitine deficiency, and hypokalemic patients may be given potassium.1,6,7 These patients will also need counseling before they consider engaging in an exercise program.
Patient’s Outcome
The case patient presented with exertional rhabdomyolysis; improper hydration, severe deconditioning, and a relatively low serum potassium level may all have contributed to the muscle necrosis she experienced. She was given IV alkaline solutions and did not develop acute kidney injury. She was discharged from the hospital and at the time of this writing was awaiting outpatient follow-up.
It should be interesting to see whether the case patient experiences any further episodes of severe weakness after engaging in exercise. Her low-normal potassium level (reference range, 3.5 to 5.3 mmol/L17) warrants further follow-up, as does her mildly elevated thyroid-stimulating hormone level (reference range, 0.5 to 4.7 mcIU/mL17).
CONCLUSION
Patients with rhabdomyolysis may present with muscle aches, darkened urine, and/or weakness; an elevated CPK level confirms the diagnosis. Management is mainly conservative, with IV hydration accompanied by alkalinizing the urine and correcting any metabolic abnormalities, such as potassium deficiencies. For the few patients who experience severe acute kidney injury, renal replacement therapy may be necessary.
While most causes of rhabdomyolysis have obvious clinical scenarios, such as a crush injury, a search for muscle enzyme deficiencies, disorders of potassium homeostasis, and thyroid abnormalities is also warranted in patients who present with exertional rhabdomyolysis.
1. Huerta-Alardín AL, Varon J, Marik PE. Bench-to-bedside review: rhabdomyolysis—an overview for clinicians. Crit Care. 2005;9(2):158-169.
2. Warren JD, Blumbergs PC, Thompson PD. Rhabdomyolysis: a review. Muscle Nerve. 2002;25(3):332-347.
3. Lima RSA, da Silva GB Jr, Liborio AB, Daher ED. Acute kidney injury due to rhabdomyolysis. Saudi J Kidney Dis Transpl. 2008;19(5):721-729.
4. Bywaters EG, Beall D. Crush injuries with impairment of renal function [reprinted from BMJ, 1941]. J Am Soc Nephrol. 1998;9(2):322-332.
5. Vanholder R, Van Biesen W, Lameire N, Sever MS; International Society of Nephrology/Renal Disaster Relief Task Force. The role of the International Society of Nephrology/Renal Disaster Relief Task Force in the rescue of renal disaster victims. Contrib Nephrol. 2007;156:325-332.
6. Toledo R, López V, Martín G, et al. Rhabdomyolysis due to enzyme deficiency in muscles. Nefrología. 2009;29(1):77-80.
7. Agrawal S, Agrawal V, Taneja A. Hypokalemia causing rhabdomyolysis resulting in life-threatening hyperkalemia. Pediatr Nephrol. 2006;221(2): 289-291.
8. Knochel JP, Schlein EM. On the mechanism of rhabdomyolysis in potassium depletion. J Clin Invest. 1972:51(7):1750-1758.
9. Knochel JP. Hypophosphatemia and rhabdomyolysis. Am J Med. 1992;92(5):455-457.
10. Mansi IA, Huang J. Rhabdomyolysis in response to weight-loss herbal medicine. Am J Med Sci. 2004; 327(6): 356-357.
11. Heber D, Yip I, Ashley JM, et al. Cholesterol-lowering effects of a proprietary Chinese red-yeast-rice dietary supplement. Am J Clin Nutr. 1999;69(2): 231-236.
12. Hooda AK, Narula AS. Exertional rhabdomyolysis causing acute renal failure. Med J Armed Forces India. 2005;61(4):395-396.
13. Chatzizisis YS, Misirli G, Hatzitolios AI, Giannoglou GD. The syndrome of rhabdomyolysis: complications and treatment. Eur J Intern Med. 2008;19(8): 568-574.
14. Blanco JR, Zabalza M, Salcedo J, et al. Rhabdomyolysis of infectious and noninfectious causes. South Med J. 2002;95(5):542-544.
15. Ron D, Taitelman U, Michaelson M, et al. Prevention of acute renal failure in traumatic rhabdomyolysis. Arch Intern Med. 1984;144(2):277-280.
16. Soni SS, Nagarik AP, Adikey GK, Raman A. Using continuous renal replacement therapy to manage patients of shock and acute renal failure. J Emerg Trauma Shock. 2009;2(1):19-22.
17. Normal laboratory values. In: Beers MH, Berkow R, eds. The Merck Manual of Diagnosis and Therapy. 17th ed. Whitehouse Station, NJ: Merck Research Laboratories; 1999:2526-2546.
1. Huerta-Alardín AL, Varon J, Marik PE. Bench-to-bedside review: rhabdomyolysis—an overview for clinicians. Crit Care. 2005;9(2):158-169.
2. Warren JD, Blumbergs PC, Thompson PD. Rhabdomyolysis: a review. Muscle Nerve. 2002;25(3):332-347.
3. Lima RSA, da Silva GB Jr, Liborio AB, Daher ED. Acute kidney injury due to rhabdomyolysis. Saudi J Kidney Dis Transpl. 2008;19(5):721-729.
4. Bywaters EG, Beall D. Crush injuries with impairment of renal function [reprinted from BMJ, 1941]. J Am Soc Nephrol. 1998;9(2):322-332.
5. Vanholder R, Van Biesen W, Lameire N, Sever MS; International Society of Nephrology/Renal Disaster Relief Task Force. The role of the International Society of Nephrology/Renal Disaster Relief Task Force in the rescue of renal disaster victims. Contrib Nephrol. 2007;156:325-332.
6. Toledo R, López V, Martín G, et al. Rhabdomyolysis due to enzyme deficiency in muscles. Nefrología. 2009;29(1):77-80.
7. Agrawal S, Agrawal V, Taneja A. Hypokalemia causing rhabdomyolysis resulting in life-threatening hyperkalemia. Pediatr Nephrol. 2006;221(2): 289-291.
8. Knochel JP, Schlein EM. On the mechanism of rhabdomyolysis in potassium depletion. J Clin Invest. 1972:51(7):1750-1758.
9. Knochel JP. Hypophosphatemia and rhabdomyolysis. Am J Med. 1992;92(5):455-457.
10. Mansi IA, Huang J. Rhabdomyolysis in response to weight-loss herbal medicine. Am J Med Sci. 2004; 327(6): 356-357.
11. Heber D, Yip I, Ashley JM, et al. Cholesterol-lowering effects of a proprietary Chinese red-yeast-rice dietary supplement. Am J Clin Nutr. 1999;69(2): 231-236.
12. Hooda AK, Narula AS. Exertional rhabdomyolysis causing acute renal failure. Med J Armed Forces India. 2005;61(4):395-396.
13. Chatzizisis YS, Misirli G, Hatzitolios AI, Giannoglou GD. The syndrome of rhabdomyolysis: complications and treatment. Eur J Intern Med. 2008;19(8): 568-574.
14. Blanco JR, Zabalza M, Salcedo J, et al. Rhabdomyolysis of infectious and noninfectious causes. South Med J. 2002;95(5):542-544.
15. Ron D, Taitelman U, Michaelson M, et al. Prevention of acute renal failure in traumatic rhabdomyolysis. Arch Intern Med. 1984;144(2):277-280.
16. Soni SS, Nagarik AP, Adikey GK, Raman A. Using continuous renal replacement therapy to manage patients of shock and acute renal failure. J Emerg Trauma Shock. 2009;2(1):19-22.
17. Normal laboratory values. In: Beers MH, Berkow R, eds. The Merck Manual of Diagnosis and Therapy. 17th ed. Whitehouse Station, NJ: Merck Research Laboratories; 1999:2526-2546.
Hospital-Acquired and Community-Acquired MRSA: Two Distinct Infections
Cocaine-Associated Chest Pain
Update on Kidney Stones
Acetabular Component Revision in Total Hip Arthroplasty. Part I: Cementless Shells
Afraid of getting sued? A plaintiff attorney offers counsel (but no sympathy)
No surprise that the lawyer who wrote Sue the Doctor and Win! has a divergent view of the medical liability “crisis,” compared with the way ObGyns usually see it.
Lewis Laska, JD, PhD, shares ObGyns’ concerns about the effect of malpractice on women and their children. But he doesn’t agree that the number of lawsuits is increasing, or that the dollar value of jury verdicts is rising beyond what might be expected with “normal” inflation, or that most malpractice cases are generated by “greedy” lawyers.
Instead, he asserts that most liability cases arise from poor care, that ObGyns and other physicians often do themselves more harm than good when responding to a poor outcome, and that all doctors could learn a lot by considering the viewpoint of their nemesis, the trial attorney.
OBG Management decided to explore Dr. Laska’s intriguing proposition to view medical malpractice through an alternative lens and take advantage of his considerable experience as an attorney and medical malpractice expert. In a Q&A session, we asked about some of his assertions and inquired specifically about the ways he believes physicians draw avoidable medicolegal trouble.
Dr. Laska is a legal consultant and editor of Medical Malpractice Verdicts, Settlements & Experts, a monthly compendium of malpractice cases from around the country (www.verdictslaska.com) and the sole source of malpractice case summaries in the “Medical Verdicts”
OBG MANAGEMENT: Let’s focus first on the fundamental disagreements between malpractice attorneys and physicians. In your opinion, what are the most common misconceptions among ObGyns about malpractice litigation? That is, what do doctors just not “get” about the reasons they get sued?
LEWIS LASKA: They think that lawyers are always looking for ways to sue doctors; in reality, it’s just the opposite. For every lawsuit filed, as many as 100 are turned down. There are a lot of angry people out there, and trial lawyers do a lot of filtering.
Doctors also have the attitude that malpractice lawsuits are caused by lawyers rather than by anything that the doctor did or failed to do. In other words, physicians seem to think that health-care safety would improve if only there were no lawyers—and they overlook the obvious: that somebody (a nurse or doctor) did something wrong.
The most common misconception among ObGyns is that there is nothing they can do to avoid being sued. In reality, however, there is much that can be done. If ObGyns participated in drills to manage shoulder dystocia and common emergencies, and honed their skills and those of labor and delivery nurses so that their responses to these so-called complications were improved, they wouldn’t get sued so often.
ObGyns also fail to manage gestational diabetes aggressively, a clearly avoidable “complication.” Finally, if ObGyns were more responsive to questions from their patients, and acted more kindly, patients wouldn’t be so eager to sue them.
Is the number of lawsuits rising?
OBG MANAGEMENT: How many malpractice cases are filed each year in the United States?
LASKA: No one except the insurance companies knows how many malpractice cases are filed—and they aren’t telling. There is no central source in this country in which lawsuit filings are tallied, although some years ago the Physician Insurers Association of America cited an estimate of 30,000.
Nor is there clear agreement about what constitutes a malpractice “case.” Does it include a fall from a hospital bed? A fall from an ObGyn’s examining table?
It also is important, in addressing this question, to point out that a lawsuit is not the same thing as a claim. The latter may involve a patient simply complaining about poor treatment, bad office staff, and so on. Although a lawsuit is certainly a claim, a claim is not a lawsuit—and there are many, many more claims than lawsuits.
OBG MANAGEMENT: Is the number of malpractice lawsuits increasing?
LASKA: The most recent data that address this question are from the year 2006 and come from the National Practitioner Data Bank (NPDB). There were 15,843 medical malpractice payment reports received that year. That figure is 8.3% less than the number received in 2005, which showed a 2.2% decrease from 2004.1
Anecdotal data provide additional evidence that the number of malpractice lawsuits is dropping. For example, Massachusetts Lawyers Weekly reported that 485 lawsuits were filed in 2008, compared with 708 in 2000. And Pennsylvania Lawyers Weekly noted that 1,602 lawsuits were filed in 2008, compared with 1,641 in 2007 and 2,732 in 2002.
As for the number of lawsuits filed each year, I think the 30,000 figure is about right. According to the NPDB, the average delay between an incident that leads to payment and the payment itself is 4.88 years—and that delay actually increased by 80% from 2005 to 2006.1 If we assume that 30,000 cases are filed each year, and that it takes about 5 years for a case to close, that means about 15,843 payments each year, since it is a cumulative number for about 5 years’ worth of cases.
OBG MANAGEMENT: What about the dollar amount of jury verdicts? Has that been increasing in recent years?
LASKA: My impression is that any increase in the amount of dollars awarded simply reflects medical inflation—namely, the increase in the cost of medical care. This is especially true when the lawsuit involves future medical care, as in the case of a baby injured by health-care negligence.
Accurate dollar data are very hard to find. According to the NPDB, obstetrics-related cases generated 8.7% of all payments reported in 2006, and also were responsible for the highest median payment: $333,334.1
When discussing dollar data, it is important to avoid the use of averages because a few very high outcomes distort this figure—and most of these amounts are lowered on appeal or settled for much less on appeal. The better figure is the median, which I cited above.
OBG MANAGEMENT: In your book, you make frequent reference to ACOG Technical Bulletin #163, which no longer exists, but which was modified slightly and rearticulated in the 2003 publication, Neonatal Encephalopathy and Cerebral Palsy: Defining the Pathogenesis and Pathophysiology, as you also note.4
The 2003 report was authored by both ACOG and the American Academy of Pediatrics (AAP). In a press release issued at the time of publication, ACOG noted that newborn encephalopathy and cerebral palsy (CP) are “associated with significant mortality rates and long-term morbidity and have been central in the assignment of blame in obstetric litigation.”
In the 2003 report, ACOG and the AAP essentially concluded that the majority of newborn brain injury cases do not occur during labor and delivery, but are attributable to events that occur before labor begins.
What do you make of their stance on the matter?
LASKA: First published in 1992, Technical Bulletin #163 set a very high standard for when intrapartum asphyxia could provide a “plausible link” to CP. Criteria included:
- umbilical cord pH <7 (i.e., acidosis)
- an Apgar score of 0 to 3 that persists for more than 5 minutes
- later documentation of neonatal neurologic problems, such as seizures
- dysfunction in any or all of the newborn’s cardiovascular, gastrointestinal, hematologic, pulmonary, or renal systems.
These criteria applied only to term newborns who did not have an obvious, or, at least, diagnosable, congenital anomaly. The actual diagnosis of “the problem” caused by “the incident” was hypoxic-ischemic encephalopathy (HIE).
The main thrust of Technical Bulletin #163 was challenged in the medical literature as early as 1995, by Goodlin, who argued that the practical effect would be that few cases of CP would be judged to be the result of perinatal asphyxia.5 Two other articles by Korst described cases in which it was clear that the newborn had experienced an acute intrapartum event such as uterine rupture or a prolapsed cord, yet only one met the ACOG criteria for HIE. Korst’s later study of 47 newborns found that only 10 met all four criteria.6
The 2003 international consensus statement is similar to Technical Bulletin #163, but actually supports some of the theories in plaintiffs’ recoveries in these cases, mentioning (as #163 does not), a “sudden, rapid and sustained deterioration of the fetal heart rate pattern, usually following the sentinel event, even where the pattern was previously normal.” This statement actually endorses electronic fetal monitoring, which is commonly disparaged in litigation in the United States, despite its use in 80% of labors in this country.
An international consensus statement published in 1999 also requires “early imaging evidence of acute cerebral abnormality.”7 This means that CP can (and must) be confirmed by neuroimaging—another battleground issue in litigation in the United States.
Even your own journal recently asked who or what test can conclusively eliminate intrapartum asphyxia as a medically probable cause of cerebral palsy.8 In reply, the article stated, “The answers are disheartening.” The article went on to explain that “only 14.5% of CP cases are associated with intrapartum asphyxia.” Let’s see. That would mean 14.5% of 6,400 cases of CP—or 928 needlessly brain-damaged infants each year.
My personal view is that the percentage of CP cases caused by an intrapartum event is higher than currently thought.
Why are so many cases settled?
OBG MANAGEMENT: In your book, you note the following:
In 1994, it was reported by American Medical News, the AMA’s weekly newspaper, that of every 100 birth-injury lawsuits filed, 47 were dropped by the plaintiffs or dismissed by the court prior to trial. Of the remaining 53 cases, 40 (three quarters) were settled by monetary payment. That leaves 13 cases. Of these, the doctor won 78%. In other words, plaintiffs won only three of the 13 that went to trial. This means that only 3% of birth injury cases result in a plaintiff‘s verdict.2
Are these figures still relatively accurate?
LASKA: Yes, so far as I can tell.
OBG MANAGEMENT: Why do you think so many cases (40%) are settled by monetary payment? Is there blatant negligence in those cases? Or is the insurance company simply reluctant to bear the burden of cost of seeing the case all the way to trial?
LASKA: Sorry, but this is a false dichotomy. Insurance companies never settle unless there is provable liability. The notion that an insurance company would settle a big injury case with marginal liability is simply a cultural myth of medicine.
OBG MANAGEMENT: In your book, you say many injured patients sue just to find out what really went wrong because the doctor has not been communicative about all the events that transpired. If physicians were more straightforward about adverse outcomes and the reasons for them, do you think fewer patients would sue?
LASKA: Yes, I think there would be fewer suits, lower settlements, and greater trust. Doctors should stop demanding “tort reform” and look more closely at themselves.
If my book seems too toxic for ObGyns, another option is Medical Errors and Medical Narcissism by John D. Banja. He argues that physicians are self-obsessed, wanting to be seen as “perfect.” And when they do wrong, they follow a path driven by narcissism. Shock and concern are followed by rationalization, avoidance, and minimization.
By the way, most people would like doctors to communicate with them the way physicians communicate with patients (and one another) on television. Jurors are sometimes stunned to learn that the doctor being sued did not communicate with nurses about the problem as it arose, and then disappeared without talking to the injured patient.
OBG MANAGEMENT: You say that about one in eight patients who sustain injury in the hospital actually sues. Why do you think that figure is so low?
LASKA: The injuries sustained are not so severe that a lawyer can be convinced to take the case, or the patient simply does not know that she was injured by negligence.
Because it takes so much money to press a health-care liability case, the injury has to be severe to justify it. Here’s an example: The obstetrician cuts the baby’s face during a cesarean delivery. The parents are outraged, but if the baby heals nicely, there really isn’t much of a case that will bring enough money from a jury to justify a lawsuit.
OBG MANAGEMENT: In your book, you claim that juries are moved not by sympathy, but by anger. Could you elaborate?
LASKA: When a physician is sued, and, in response, points the finger at someone else, who points the finger right back, juries conclude that the team simply was not working together. And the refusal of anyone on that team to accept responsibility makes the jury angry. Doctors may call it “system breakdown,” but juries consider it malpractice—or, the term I now use, “health-care liability.”
Another reason juries get angry is the rude and condescending behavior that physicians sometimes exhibit in videotaped testimony. Sometimes doctors make fools of themselves in these videotapes by contradicting themselves, contradicting the medical records, contradicting the testimony of nurses, and so on. This kind of behavior will torpedo a case and lead to a higher verdict than it would have in the days before videotaping, when the deposition was merely read to the jury.
How do lawyers try these cases?
OBG MANAGEMENT: Has the way in which lawyers try cases changed?
LASKA: Most medical liability cases now end up in the hands of legal “specialists,” who have experience in a particular area. In addition, lawyers now share information better than in the past. ObGyns and other doctors don’t understand that health-care victims’ lawyers are working together as never before and learning to overcome the many defenses—some very tenuous—that are raised in a doctor’s defense.
A recent Tennessee case is an example. In Olinger v. University Medical Center, the defendant ObGyn (and his experts) testified that shoulder dystocia is a “sudden emergency” because it occurs in only 3% of deliveries.3 They also asserted that 90% of the time, shoulder dystocia is relieved by initial maneuvers, such as McRoberts’ maneuver.
In this case, because the doctor had delivered 4,000 babies and had encountered shoulder dystocia only 100 times, and because the legal case represented the first time initial maneuvers had failed to resolve the dystocia, the defense argued that the occurrence was a true “sudden emergency,” allowing the jury to be so instructed on that issue.
The doctor won his case—fine. But now that it is established in Tennessee law and Tennessee medicine that shoulder dystocia that cannot be resolved with “initial maneuvers” is a medical emergency, you can bet that victims’ lawyers are going to find ways to demonstrate that a particular case is one in which the doctor did not know how to deal with this particular “sudden emergency.” In short, the Olinger case provides a roadmap for how to win (or turn down) a shoulder dystocia case.
OBG MANAGEMENT: What do you think about proposals set forth to resolve the malpractice crisis?
LASKA: In the 1970s, physicians advocated malpractice review panels to end the so-called crisis. These panels fell from favor because they did not work. Now, the idea du jour is the establishment of special “malpractice courts.”
What will be the result? A cadre of superspecialists will develop who handle nothing but malpractice court cases. The typical lawyer will refer cases to one of these superspecialists (as they usually do now), and it will become easier to prove the standard of care nationwide. After all, why should the handling of a case involving shoulder dystocia be different in Phoenix than it is in Nashville?
Doctors, be careful what you wish for. Special malpractice courts are the first step toward national standards of care.
OBG MANAGEMENT: A final question: Who buys your book, Sue the Doctor and Win!, as far as you are able to gauge?
LASKA: The primary buyers have been MD/JDs, probably because they all wanted to write such a book. Nurse consultants have also been buying it, as well as “puppy” lawyers at malpractice firms.
By the way, the book has sold poorly. Everybody thinks they already know all they need to know about malpractice. That includes doctors and victim’s lawyers.
f
1. National Practitioner Data Bank 2006 Annual Report. US Department of Health and Human Services. Health Resources and Services Administration. Bureau of Health Professions, Division of Practitioner Data Banks. Available at: http://www.npdb-hipdb.hrsa.gov/pubs/stats/2006_NPDB_Annual_Report.pdf. Accessed September 16, 2009.
2. Laska L. Sue the doctor and win! Victim’s guide to secrets of malpractice lawsuits. Nashville, TN: Farmacon Press; 2007.
3. 269 SW3d 560 (Tenn App 2008).
4. American College of Obstetricians and Gynecologists American Academy of Pediatrics. Neonatal encephalopathy and cerebral palsy: defining the pathogenesis and pathophysiology. Washington, DC: ACOG; 2003.
5. Goodlin RC. Do concepts of causes and prevention of cerebral palsy require revision? Am J Obstet Gynecol. 1995;172:1830-1836.
6. Korst LM, Phelan JP, Wang YM, Martin GI, Ahn MO. Acute fetal asphyxia and permanent brain injury: a retrospective analysis of current indicators. J Matern Fetal Med. 1999;8(3):101-106.
7. MacLennan A. A template for defining a causal relation between acute intrapartum events and cerebral palsy: international consensus statement. BMJ. 1999;319:1054-1059.
8. Repke JT. What percentage of cerebral palsy cases might be associated with intrapartum asphyxia? Examining the Evidence. OBG Management. 2009;21(3):15-16.
No surprise that the lawyer who wrote Sue the Doctor and Win! has a divergent view of the medical liability “crisis,” compared with the way ObGyns usually see it.
Lewis Laska, JD, PhD, shares ObGyns’ concerns about the effect of malpractice on women and their children. But he doesn’t agree that the number of lawsuits is increasing, or that the dollar value of jury verdicts is rising beyond what might be expected with “normal” inflation, or that most malpractice cases are generated by “greedy” lawyers.
Instead, he asserts that most liability cases arise from poor care, that ObGyns and other physicians often do themselves more harm than good when responding to a poor outcome, and that all doctors could learn a lot by considering the viewpoint of their nemesis, the trial attorney.
OBG Management decided to explore Dr. Laska’s intriguing proposition to view medical malpractice through an alternative lens and take advantage of his considerable experience as an attorney and medical malpractice expert. In a Q&A session, we asked about some of his assertions and inquired specifically about the ways he believes physicians draw avoidable medicolegal trouble.
Dr. Laska is a legal consultant and editor of Medical Malpractice Verdicts, Settlements & Experts, a monthly compendium of malpractice cases from around the country (www.verdictslaska.com) and the sole source of malpractice case summaries in the “Medical Verdicts”
OBG MANAGEMENT: Let’s focus first on the fundamental disagreements between malpractice attorneys and physicians. In your opinion, what are the most common misconceptions among ObGyns about malpractice litigation? That is, what do doctors just not “get” about the reasons they get sued?
LEWIS LASKA: They think that lawyers are always looking for ways to sue doctors; in reality, it’s just the opposite. For every lawsuit filed, as many as 100 are turned down. There are a lot of angry people out there, and trial lawyers do a lot of filtering.
Doctors also have the attitude that malpractice lawsuits are caused by lawyers rather than by anything that the doctor did or failed to do. In other words, physicians seem to think that health-care safety would improve if only there were no lawyers—and they overlook the obvious: that somebody (a nurse or doctor) did something wrong.
The most common misconception among ObGyns is that there is nothing they can do to avoid being sued. In reality, however, there is much that can be done. If ObGyns participated in drills to manage shoulder dystocia and common emergencies, and honed their skills and those of labor and delivery nurses so that their responses to these so-called complications were improved, they wouldn’t get sued so often.
ObGyns also fail to manage gestational diabetes aggressively, a clearly avoidable “complication.” Finally, if ObGyns were more responsive to questions from their patients, and acted more kindly, patients wouldn’t be so eager to sue them.
Is the number of lawsuits rising?
OBG MANAGEMENT: How many malpractice cases are filed each year in the United States?
LASKA: No one except the insurance companies knows how many malpractice cases are filed—and they aren’t telling. There is no central source in this country in which lawsuit filings are tallied, although some years ago the Physician Insurers Association of America cited an estimate of 30,000.
Nor is there clear agreement about what constitutes a malpractice “case.” Does it include a fall from a hospital bed? A fall from an ObGyn’s examining table?
It also is important, in addressing this question, to point out that a lawsuit is not the same thing as a claim. The latter may involve a patient simply complaining about poor treatment, bad office staff, and so on. Although a lawsuit is certainly a claim, a claim is not a lawsuit—and there are many, many more claims than lawsuits.
OBG MANAGEMENT: Is the number of malpractice lawsuits increasing?
LASKA: The most recent data that address this question are from the year 2006 and come from the National Practitioner Data Bank (NPDB). There were 15,843 medical malpractice payment reports received that year. That figure is 8.3% less than the number received in 2005, which showed a 2.2% decrease from 2004.1
Anecdotal data provide additional evidence that the number of malpractice lawsuits is dropping. For example, Massachusetts Lawyers Weekly reported that 485 lawsuits were filed in 2008, compared with 708 in 2000. And Pennsylvania Lawyers Weekly noted that 1,602 lawsuits were filed in 2008, compared with 1,641 in 2007 and 2,732 in 2002.
As for the number of lawsuits filed each year, I think the 30,000 figure is about right. According to the NPDB, the average delay between an incident that leads to payment and the payment itself is 4.88 years—and that delay actually increased by 80% from 2005 to 2006.1 If we assume that 30,000 cases are filed each year, and that it takes about 5 years for a case to close, that means about 15,843 payments each year, since it is a cumulative number for about 5 years’ worth of cases.
OBG MANAGEMENT: What about the dollar amount of jury verdicts? Has that been increasing in recent years?
LASKA: My impression is that any increase in the amount of dollars awarded simply reflects medical inflation—namely, the increase in the cost of medical care. This is especially true when the lawsuit involves future medical care, as in the case of a baby injured by health-care negligence.
Accurate dollar data are very hard to find. According to the NPDB, obstetrics-related cases generated 8.7% of all payments reported in 2006, and also were responsible for the highest median payment: $333,334.1
When discussing dollar data, it is important to avoid the use of averages because a few very high outcomes distort this figure—and most of these amounts are lowered on appeal or settled for much less on appeal. The better figure is the median, which I cited above.
OBG MANAGEMENT: In your book, you make frequent reference to ACOG Technical Bulletin #163, which no longer exists, but which was modified slightly and rearticulated in the 2003 publication, Neonatal Encephalopathy and Cerebral Palsy: Defining the Pathogenesis and Pathophysiology, as you also note.4
The 2003 report was authored by both ACOG and the American Academy of Pediatrics (AAP). In a press release issued at the time of publication, ACOG noted that newborn encephalopathy and cerebral palsy (CP) are “associated with significant mortality rates and long-term morbidity and have been central in the assignment of blame in obstetric litigation.”
In the 2003 report, ACOG and the AAP essentially concluded that the majority of newborn brain injury cases do not occur during labor and delivery, but are attributable to events that occur before labor begins.
What do you make of their stance on the matter?
LASKA: First published in 1992, Technical Bulletin #163 set a very high standard for when intrapartum asphyxia could provide a “plausible link” to CP. Criteria included:
- umbilical cord pH <7 (i.e., acidosis)
- an Apgar score of 0 to 3 that persists for more than 5 minutes
- later documentation of neonatal neurologic problems, such as seizures
- dysfunction in any or all of the newborn’s cardiovascular, gastrointestinal, hematologic, pulmonary, or renal systems.
These criteria applied only to term newborns who did not have an obvious, or, at least, diagnosable, congenital anomaly. The actual diagnosis of “the problem” caused by “the incident” was hypoxic-ischemic encephalopathy (HIE).
The main thrust of Technical Bulletin #163 was challenged in the medical literature as early as 1995, by Goodlin, who argued that the practical effect would be that few cases of CP would be judged to be the result of perinatal asphyxia.5 Two other articles by Korst described cases in which it was clear that the newborn had experienced an acute intrapartum event such as uterine rupture or a prolapsed cord, yet only one met the ACOG criteria for HIE. Korst’s later study of 47 newborns found that only 10 met all four criteria.6
The 2003 international consensus statement is similar to Technical Bulletin #163, but actually supports some of the theories in plaintiffs’ recoveries in these cases, mentioning (as #163 does not), a “sudden, rapid and sustained deterioration of the fetal heart rate pattern, usually following the sentinel event, even where the pattern was previously normal.” This statement actually endorses electronic fetal monitoring, which is commonly disparaged in litigation in the United States, despite its use in 80% of labors in this country.
An international consensus statement published in 1999 also requires “early imaging evidence of acute cerebral abnormality.”7 This means that CP can (and must) be confirmed by neuroimaging—another battleground issue in litigation in the United States.
Even your own journal recently asked who or what test can conclusively eliminate intrapartum asphyxia as a medically probable cause of cerebral palsy.8 In reply, the article stated, “The answers are disheartening.” The article went on to explain that “only 14.5% of CP cases are associated with intrapartum asphyxia.” Let’s see. That would mean 14.5% of 6,400 cases of CP—or 928 needlessly brain-damaged infants each year.
My personal view is that the percentage of CP cases caused by an intrapartum event is higher than currently thought.
Why are so many cases settled?
OBG MANAGEMENT: In your book, you note the following:
In 1994, it was reported by American Medical News, the AMA’s weekly newspaper, that of every 100 birth-injury lawsuits filed, 47 were dropped by the plaintiffs or dismissed by the court prior to trial. Of the remaining 53 cases, 40 (three quarters) were settled by monetary payment. That leaves 13 cases. Of these, the doctor won 78%. In other words, plaintiffs won only three of the 13 that went to trial. This means that only 3% of birth injury cases result in a plaintiff‘s verdict.2
Are these figures still relatively accurate?
LASKA: Yes, so far as I can tell.
OBG MANAGEMENT: Why do you think so many cases (40%) are settled by monetary payment? Is there blatant negligence in those cases? Or is the insurance company simply reluctant to bear the burden of cost of seeing the case all the way to trial?
LASKA: Sorry, but this is a false dichotomy. Insurance companies never settle unless there is provable liability. The notion that an insurance company would settle a big injury case with marginal liability is simply a cultural myth of medicine.
OBG MANAGEMENT: In your book, you say many injured patients sue just to find out what really went wrong because the doctor has not been communicative about all the events that transpired. If physicians were more straightforward about adverse outcomes and the reasons for them, do you think fewer patients would sue?
LASKA: Yes, I think there would be fewer suits, lower settlements, and greater trust. Doctors should stop demanding “tort reform” and look more closely at themselves.
If my book seems too toxic for ObGyns, another option is Medical Errors and Medical Narcissism by John D. Banja. He argues that physicians are self-obsessed, wanting to be seen as “perfect.” And when they do wrong, they follow a path driven by narcissism. Shock and concern are followed by rationalization, avoidance, and minimization.
By the way, most people would like doctors to communicate with them the way physicians communicate with patients (and one another) on television. Jurors are sometimes stunned to learn that the doctor being sued did not communicate with nurses about the problem as it arose, and then disappeared without talking to the injured patient.
OBG MANAGEMENT: You say that about one in eight patients who sustain injury in the hospital actually sues. Why do you think that figure is so low?
LASKA: The injuries sustained are not so severe that a lawyer can be convinced to take the case, or the patient simply does not know that she was injured by negligence.
Because it takes so much money to press a health-care liability case, the injury has to be severe to justify it. Here’s an example: The obstetrician cuts the baby’s face during a cesarean delivery. The parents are outraged, but if the baby heals nicely, there really isn’t much of a case that will bring enough money from a jury to justify a lawsuit.
OBG MANAGEMENT: In your book, you claim that juries are moved not by sympathy, but by anger. Could you elaborate?
LASKA: When a physician is sued, and, in response, points the finger at someone else, who points the finger right back, juries conclude that the team simply was not working together. And the refusal of anyone on that team to accept responsibility makes the jury angry. Doctors may call it “system breakdown,” but juries consider it malpractice—or, the term I now use, “health-care liability.”
Another reason juries get angry is the rude and condescending behavior that physicians sometimes exhibit in videotaped testimony. Sometimes doctors make fools of themselves in these videotapes by contradicting themselves, contradicting the medical records, contradicting the testimony of nurses, and so on. This kind of behavior will torpedo a case and lead to a higher verdict than it would have in the days before videotaping, when the deposition was merely read to the jury.
How do lawyers try these cases?
OBG MANAGEMENT: Has the way in which lawyers try cases changed?
LASKA: Most medical liability cases now end up in the hands of legal “specialists,” who have experience in a particular area. In addition, lawyers now share information better than in the past. ObGyns and other doctors don’t understand that health-care victims’ lawyers are working together as never before and learning to overcome the many defenses—some very tenuous—that are raised in a doctor’s defense.
A recent Tennessee case is an example. In Olinger v. University Medical Center, the defendant ObGyn (and his experts) testified that shoulder dystocia is a “sudden emergency” because it occurs in only 3% of deliveries.3 They also asserted that 90% of the time, shoulder dystocia is relieved by initial maneuvers, such as McRoberts’ maneuver.
In this case, because the doctor had delivered 4,000 babies and had encountered shoulder dystocia only 100 times, and because the legal case represented the first time initial maneuvers had failed to resolve the dystocia, the defense argued that the occurrence was a true “sudden emergency,” allowing the jury to be so instructed on that issue.
The doctor won his case—fine. But now that it is established in Tennessee law and Tennessee medicine that shoulder dystocia that cannot be resolved with “initial maneuvers” is a medical emergency, you can bet that victims’ lawyers are going to find ways to demonstrate that a particular case is one in which the doctor did not know how to deal with this particular “sudden emergency.” In short, the Olinger case provides a roadmap for how to win (or turn down) a shoulder dystocia case.
OBG MANAGEMENT: What do you think about proposals set forth to resolve the malpractice crisis?
LASKA: In the 1970s, physicians advocated malpractice review panels to end the so-called crisis. These panels fell from favor because they did not work. Now, the idea du jour is the establishment of special “malpractice courts.”
What will be the result? A cadre of superspecialists will develop who handle nothing but malpractice court cases. The typical lawyer will refer cases to one of these superspecialists (as they usually do now), and it will become easier to prove the standard of care nationwide. After all, why should the handling of a case involving shoulder dystocia be different in Phoenix than it is in Nashville?
Doctors, be careful what you wish for. Special malpractice courts are the first step toward national standards of care.
OBG MANAGEMENT: A final question: Who buys your book, Sue the Doctor and Win!, as far as you are able to gauge?
LASKA: The primary buyers have been MD/JDs, probably because they all wanted to write such a book. Nurse consultants have also been buying it, as well as “puppy” lawyers at malpractice firms.
By the way, the book has sold poorly. Everybody thinks they already know all they need to know about malpractice. That includes doctors and victim’s lawyers.
f
No surprise that the lawyer who wrote Sue the Doctor and Win! has a divergent view of the medical liability “crisis,” compared with the way ObGyns usually see it.
Lewis Laska, JD, PhD, shares ObGyns’ concerns about the effect of malpractice on women and their children. But he doesn’t agree that the number of lawsuits is increasing, or that the dollar value of jury verdicts is rising beyond what might be expected with “normal” inflation, or that most malpractice cases are generated by “greedy” lawyers.
Instead, he asserts that most liability cases arise from poor care, that ObGyns and other physicians often do themselves more harm than good when responding to a poor outcome, and that all doctors could learn a lot by considering the viewpoint of their nemesis, the trial attorney.
OBG Management decided to explore Dr. Laska’s intriguing proposition to view medical malpractice through an alternative lens and take advantage of his considerable experience as an attorney and medical malpractice expert. In a Q&A session, we asked about some of his assertions and inquired specifically about the ways he believes physicians draw avoidable medicolegal trouble.
Dr. Laska is a legal consultant and editor of Medical Malpractice Verdicts, Settlements & Experts, a monthly compendium of malpractice cases from around the country (www.verdictslaska.com) and the sole source of malpractice case summaries in the “Medical Verdicts”
OBG MANAGEMENT: Let’s focus first on the fundamental disagreements between malpractice attorneys and physicians. In your opinion, what are the most common misconceptions among ObGyns about malpractice litigation? That is, what do doctors just not “get” about the reasons they get sued?
LEWIS LASKA: They think that lawyers are always looking for ways to sue doctors; in reality, it’s just the opposite. For every lawsuit filed, as many as 100 are turned down. There are a lot of angry people out there, and trial lawyers do a lot of filtering.
Doctors also have the attitude that malpractice lawsuits are caused by lawyers rather than by anything that the doctor did or failed to do. In other words, physicians seem to think that health-care safety would improve if only there were no lawyers—and they overlook the obvious: that somebody (a nurse or doctor) did something wrong.
The most common misconception among ObGyns is that there is nothing they can do to avoid being sued. In reality, however, there is much that can be done. If ObGyns participated in drills to manage shoulder dystocia and common emergencies, and honed their skills and those of labor and delivery nurses so that their responses to these so-called complications were improved, they wouldn’t get sued so often.
ObGyns also fail to manage gestational diabetes aggressively, a clearly avoidable “complication.” Finally, if ObGyns were more responsive to questions from their patients, and acted more kindly, patients wouldn’t be so eager to sue them.
Is the number of lawsuits rising?
OBG MANAGEMENT: How many malpractice cases are filed each year in the United States?
LASKA: No one except the insurance companies knows how many malpractice cases are filed—and they aren’t telling. There is no central source in this country in which lawsuit filings are tallied, although some years ago the Physician Insurers Association of America cited an estimate of 30,000.
Nor is there clear agreement about what constitutes a malpractice “case.” Does it include a fall from a hospital bed? A fall from an ObGyn’s examining table?
It also is important, in addressing this question, to point out that a lawsuit is not the same thing as a claim. The latter may involve a patient simply complaining about poor treatment, bad office staff, and so on. Although a lawsuit is certainly a claim, a claim is not a lawsuit—and there are many, many more claims than lawsuits.
OBG MANAGEMENT: Is the number of malpractice lawsuits increasing?
LASKA: The most recent data that address this question are from the year 2006 and come from the National Practitioner Data Bank (NPDB). There were 15,843 medical malpractice payment reports received that year. That figure is 8.3% less than the number received in 2005, which showed a 2.2% decrease from 2004.1
Anecdotal data provide additional evidence that the number of malpractice lawsuits is dropping. For example, Massachusetts Lawyers Weekly reported that 485 lawsuits were filed in 2008, compared with 708 in 2000. And Pennsylvania Lawyers Weekly noted that 1,602 lawsuits were filed in 2008, compared with 1,641 in 2007 and 2,732 in 2002.
As for the number of lawsuits filed each year, I think the 30,000 figure is about right. According to the NPDB, the average delay between an incident that leads to payment and the payment itself is 4.88 years—and that delay actually increased by 80% from 2005 to 2006.1 If we assume that 30,000 cases are filed each year, and that it takes about 5 years for a case to close, that means about 15,843 payments each year, since it is a cumulative number for about 5 years’ worth of cases.
OBG MANAGEMENT: What about the dollar amount of jury verdicts? Has that been increasing in recent years?
LASKA: My impression is that any increase in the amount of dollars awarded simply reflects medical inflation—namely, the increase in the cost of medical care. This is especially true when the lawsuit involves future medical care, as in the case of a baby injured by health-care negligence.
Accurate dollar data are very hard to find. According to the NPDB, obstetrics-related cases generated 8.7% of all payments reported in 2006, and also were responsible for the highest median payment: $333,334.1
When discussing dollar data, it is important to avoid the use of averages because a few very high outcomes distort this figure—and most of these amounts are lowered on appeal or settled for much less on appeal. The better figure is the median, which I cited above.
OBG MANAGEMENT: In your book, you make frequent reference to ACOG Technical Bulletin #163, which no longer exists, but which was modified slightly and rearticulated in the 2003 publication, Neonatal Encephalopathy and Cerebral Palsy: Defining the Pathogenesis and Pathophysiology, as you also note.4
The 2003 report was authored by both ACOG and the American Academy of Pediatrics (AAP). In a press release issued at the time of publication, ACOG noted that newborn encephalopathy and cerebral palsy (CP) are “associated with significant mortality rates and long-term morbidity and have been central in the assignment of blame in obstetric litigation.”
In the 2003 report, ACOG and the AAP essentially concluded that the majority of newborn brain injury cases do not occur during labor and delivery, but are attributable to events that occur before labor begins.
What do you make of their stance on the matter?
LASKA: First published in 1992, Technical Bulletin #163 set a very high standard for when intrapartum asphyxia could provide a “plausible link” to CP. Criteria included:
- umbilical cord pH <7 (i.e., acidosis)
- an Apgar score of 0 to 3 that persists for more than 5 minutes
- later documentation of neonatal neurologic problems, such as seizures
- dysfunction in any or all of the newborn’s cardiovascular, gastrointestinal, hematologic, pulmonary, or renal systems.
These criteria applied only to term newborns who did not have an obvious, or, at least, diagnosable, congenital anomaly. The actual diagnosis of “the problem” caused by “the incident” was hypoxic-ischemic encephalopathy (HIE).
The main thrust of Technical Bulletin #163 was challenged in the medical literature as early as 1995, by Goodlin, who argued that the practical effect would be that few cases of CP would be judged to be the result of perinatal asphyxia.5 Two other articles by Korst described cases in which it was clear that the newborn had experienced an acute intrapartum event such as uterine rupture or a prolapsed cord, yet only one met the ACOG criteria for HIE. Korst’s later study of 47 newborns found that only 10 met all four criteria.6
The 2003 international consensus statement is similar to Technical Bulletin #163, but actually supports some of the theories in plaintiffs’ recoveries in these cases, mentioning (as #163 does not), a “sudden, rapid and sustained deterioration of the fetal heart rate pattern, usually following the sentinel event, even where the pattern was previously normal.” This statement actually endorses electronic fetal monitoring, which is commonly disparaged in litigation in the United States, despite its use in 80% of labors in this country.
An international consensus statement published in 1999 also requires “early imaging evidence of acute cerebral abnormality.”7 This means that CP can (and must) be confirmed by neuroimaging—another battleground issue in litigation in the United States.
Even your own journal recently asked who or what test can conclusively eliminate intrapartum asphyxia as a medically probable cause of cerebral palsy.8 In reply, the article stated, “The answers are disheartening.” The article went on to explain that “only 14.5% of CP cases are associated with intrapartum asphyxia.” Let’s see. That would mean 14.5% of 6,400 cases of CP—or 928 needlessly brain-damaged infants each year.
My personal view is that the percentage of CP cases caused by an intrapartum event is higher than currently thought.
Why are so many cases settled?
OBG MANAGEMENT: In your book, you note the following:
In 1994, it was reported by American Medical News, the AMA’s weekly newspaper, that of every 100 birth-injury lawsuits filed, 47 were dropped by the plaintiffs or dismissed by the court prior to trial. Of the remaining 53 cases, 40 (three quarters) were settled by monetary payment. That leaves 13 cases. Of these, the doctor won 78%. In other words, plaintiffs won only three of the 13 that went to trial. This means that only 3% of birth injury cases result in a plaintiff‘s verdict.2
Are these figures still relatively accurate?
LASKA: Yes, so far as I can tell.
OBG MANAGEMENT: Why do you think so many cases (40%) are settled by monetary payment? Is there blatant negligence in those cases? Or is the insurance company simply reluctant to bear the burden of cost of seeing the case all the way to trial?
LASKA: Sorry, but this is a false dichotomy. Insurance companies never settle unless there is provable liability. The notion that an insurance company would settle a big injury case with marginal liability is simply a cultural myth of medicine.
OBG MANAGEMENT: In your book, you say many injured patients sue just to find out what really went wrong because the doctor has not been communicative about all the events that transpired. If physicians were more straightforward about adverse outcomes and the reasons for them, do you think fewer patients would sue?
LASKA: Yes, I think there would be fewer suits, lower settlements, and greater trust. Doctors should stop demanding “tort reform” and look more closely at themselves.
If my book seems too toxic for ObGyns, another option is Medical Errors and Medical Narcissism by John D. Banja. He argues that physicians are self-obsessed, wanting to be seen as “perfect.” And when they do wrong, they follow a path driven by narcissism. Shock and concern are followed by rationalization, avoidance, and minimization.
By the way, most people would like doctors to communicate with them the way physicians communicate with patients (and one another) on television. Jurors are sometimes stunned to learn that the doctor being sued did not communicate with nurses about the problem as it arose, and then disappeared without talking to the injured patient.
OBG MANAGEMENT: You say that about one in eight patients who sustain injury in the hospital actually sues. Why do you think that figure is so low?
LASKA: The injuries sustained are not so severe that a lawyer can be convinced to take the case, or the patient simply does not know that she was injured by negligence.
Because it takes so much money to press a health-care liability case, the injury has to be severe to justify it. Here’s an example: The obstetrician cuts the baby’s face during a cesarean delivery. The parents are outraged, but if the baby heals nicely, there really isn’t much of a case that will bring enough money from a jury to justify a lawsuit.
OBG MANAGEMENT: In your book, you claim that juries are moved not by sympathy, but by anger. Could you elaborate?
LASKA: When a physician is sued, and, in response, points the finger at someone else, who points the finger right back, juries conclude that the team simply was not working together. And the refusal of anyone on that team to accept responsibility makes the jury angry. Doctors may call it “system breakdown,” but juries consider it malpractice—or, the term I now use, “health-care liability.”
Another reason juries get angry is the rude and condescending behavior that physicians sometimes exhibit in videotaped testimony. Sometimes doctors make fools of themselves in these videotapes by contradicting themselves, contradicting the medical records, contradicting the testimony of nurses, and so on. This kind of behavior will torpedo a case and lead to a higher verdict than it would have in the days before videotaping, when the deposition was merely read to the jury.
How do lawyers try these cases?
OBG MANAGEMENT: Has the way in which lawyers try cases changed?
LASKA: Most medical liability cases now end up in the hands of legal “specialists,” who have experience in a particular area. In addition, lawyers now share information better than in the past. ObGyns and other doctors don’t understand that health-care victims’ lawyers are working together as never before and learning to overcome the many defenses—some very tenuous—that are raised in a doctor’s defense.
A recent Tennessee case is an example. In Olinger v. University Medical Center, the defendant ObGyn (and his experts) testified that shoulder dystocia is a “sudden emergency” because it occurs in only 3% of deliveries.3 They also asserted that 90% of the time, shoulder dystocia is relieved by initial maneuvers, such as McRoberts’ maneuver.
In this case, because the doctor had delivered 4,000 babies and had encountered shoulder dystocia only 100 times, and because the legal case represented the first time initial maneuvers had failed to resolve the dystocia, the defense argued that the occurrence was a true “sudden emergency,” allowing the jury to be so instructed on that issue.
The doctor won his case—fine. But now that it is established in Tennessee law and Tennessee medicine that shoulder dystocia that cannot be resolved with “initial maneuvers” is a medical emergency, you can bet that victims’ lawyers are going to find ways to demonstrate that a particular case is one in which the doctor did not know how to deal with this particular “sudden emergency.” In short, the Olinger case provides a roadmap for how to win (or turn down) a shoulder dystocia case.
OBG MANAGEMENT: What do you think about proposals set forth to resolve the malpractice crisis?
LASKA: In the 1970s, physicians advocated malpractice review panels to end the so-called crisis. These panels fell from favor because they did not work. Now, the idea du jour is the establishment of special “malpractice courts.”
What will be the result? A cadre of superspecialists will develop who handle nothing but malpractice court cases. The typical lawyer will refer cases to one of these superspecialists (as they usually do now), and it will become easier to prove the standard of care nationwide. After all, why should the handling of a case involving shoulder dystocia be different in Phoenix than it is in Nashville?
Doctors, be careful what you wish for. Special malpractice courts are the first step toward national standards of care.
OBG MANAGEMENT: A final question: Who buys your book, Sue the Doctor and Win!, as far as you are able to gauge?
LASKA: The primary buyers have been MD/JDs, probably because they all wanted to write such a book. Nurse consultants have also been buying it, as well as “puppy” lawyers at malpractice firms.
By the way, the book has sold poorly. Everybody thinks they already know all they need to know about malpractice. That includes doctors and victim’s lawyers.
f
1. National Practitioner Data Bank 2006 Annual Report. US Department of Health and Human Services. Health Resources and Services Administration. Bureau of Health Professions, Division of Practitioner Data Banks. Available at: http://www.npdb-hipdb.hrsa.gov/pubs/stats/2006_NPDB_Annual_Report.pdf. Accessed September 16, 2009.
2. Laska L. Sue the doctor and win! Victim’s guide to secrets of malpractice lawsuits. Nashville, TN: Farmacon Press; 2007.
3. 269 SW3d 560 (Tenn App 2008).
4. American College of Obstetricians and Gynecologists American Academy of Pediatrics. Neonatal encephalopathy and cerebral palsy: defining the pathogenesis and pathophysiology. Washington, DC: ACOG; 2003.
5. Goodlin RC. Do concepts of causes and prevention of cerebral palsy require revision? Am J Obstet Gynecol. 1995;172:1830-1836.
6. Korst LM, Phelan JP, Wang YM, Martin GI, Ahn MO. Acute fetal asphyxia and permanent brain injury: a retrospective analysis of current indicators. J Matern Fetal Med. 1999;8(3):101-106.
7. MacLennan A. A template for defining a causal relation between acute intrapartum events and cerebral palsy: international consensus statement. BMJ. 1999;319:1054-1059.
8. Repke JT. What percentage of cerebral palsy cases might be associated with intrapartum asphyxia? Examining the Evidence. OBG Management. 2009;21(3):15-16.
1. National Practitioner Data Bank 2006 Annual Report. US Department of Health and Human Services. Health Resources and Services Administration. Bureau of Health Professions, Division of Practitioner Data Banks. Available at: http://www.npdb-hipdb.hrsa.gov/pubs/stats/2006_NPDB_Annual_Report.pdf. Accessed September 16, 2009.
2. Laska L. Sue the doctor and win! Victim’s guide to secrets of malpractice lawsuits. Nashville, TN: Farmacon Press; 2007.
3. 269 SW3d 560 (Tenn App 2008).
4. American College of Obstetricians and Gynecologists American Academy of Pediatrics. Neonatal encephalopathy and cerebral palsy: defining the pathogenesis and pathophysiology. Washington, DC: ACOG; 2003.
5. Goodlin RC. Do concepts of causes and prevention of cerebral palsy require revision? Am J Obstet Gynecol. 1995;172:1830-1836.
6. Korst LM, Phelan JP, Wang YM, Martin GI, Ahn MO. Acute fetal asphyxia and permanent brain injury: a retrospective analysis of current indicators. J Matern Fetal Med. 1999;8(3):101-106.
7. MacLennan A. A template for defining a causal relation between acute intrapartum events and cerebral palsy: international consensus statement. BMJ. 1999;319:1054-1059.
8. Repke JT. What percentage of cerebral palsy cases might be associated with intrapartum asphyxia? Examining the Evidence. OBG Management. 2009;21(3):15-16.