CASE REPORT
A 59-year-old man with acute onset of paralysis Richard S. Cassa, MPAS, PA-C; Axel J. Rosengart, MD, PhD, MPH
CASE A 59-year-old man presented to the ED complaining of “not feeling right” and “a thick throat.” Upon awakening that morning, he had experienced subacute onset of slurred speech, upper airway swelling, and ascending weakness of all extremities. The symptoms worsened progressively over the next 6 hours, prompting him to go to the ED. History The patient lived independently and had a history of schizoaffective disorder and hypertension. He was taking venlafaxine, risperidone, hydroxyzine, aspirin, pravastatin, and hydrochlorothiazide at home. Two weeks before this admission, the patient had lost his job as a store attendant and since then had been unable to obtain medication refills. After stopping his medication, the patient became increasingly withdrawn and inattentive to his home environment and personal hygiene. He was unable to leave his home and perform his activities of daily living. Also, he did not act on the fact that his refrigerator—filled with perishable imported food—was not working properly. In the ED, the patient was afebrile with a BP of 89/65, heart rate of 86, respirations of 32 and labored, and oxygen saturation of 91% on 2 L of supplemental oxygen via nasal cannula. Over the next 2 hours, his respiratory function declined sharply, leading first to respiratory failure requiring endotracheal intubation and mechanical ventilation, Richard S. Cassa is a chief PA in the Department of Neurology, Division of Acute Neurosciences at New York Presbyterian Hospital-Cornell in New York City. Axel J. Rosengart is director of neurocritical care and an associate professor of neurology, neuroscience, and neurosurgery at Weill Cornell Medical College in New York City.The authors have disclosed no potential conflicts of interest, financial or otherwise. DOI: 10.1097/01.JAA.0000450805.98459.e6 Copyright © 2014 American Academy of Physician Assistants
© DR. GARY GAUGLER / SCIENCE SOURCE
ABSTRACT Botulism is a neuroparalytic illness resulting from the action of a potent toxin produced by the organism Clostridium botulinum. It can present with a classic triad of clear mentation, bulbar palsy and symmetric descending paralysis. Treatment is symptomatic and includes a botulinum antitoxin. Keywords: Clostridium botulinum, Guillain-Barré syndrome, myasthenia gravis, botulism, schizoaffective disorder, paralysis
FIGURE 1. Color-enhanced scanning electron micrograph of
C. botulinum, which causes botulism
then cardiac arrest. An examination after resuscitation showed a hemodynamically and respiratory stabilized patient who was unable to open his eyes; had bilateral fixed, dilated pupils; and severe weakness of all extremities. A CT scan of the head was unrevealing. The patient was subsequently transferred to our center for further care. On arrival at our hospital, the patient was awake and alert but unable to open his eyes. He was still mechanically ventilated. He responded appropriately to yes/no questions with hand grasping, revealing full orientation and no deficits in key cognitive areas. His pupils were 5 mm, unreactive, and isocoric; he had bilateral complete ophthalmoplegia with absent oculocephalic, corneal, and gag reflexes. A motor examination identified severe proximal 1/5 and distal 3/5 symmetric weakness of all extremities with normal muscle bulge and tone but absent reflexes and no Babinski signs. Sensation was intact to all modalities. He had no skin lesions. Cardiorespiratory and abdominal examinations were within normal limits. Routine blood work was normal, including liver function tests and thyroid panel. The patient’s erythrocyte sedimentation rate was 14 mm/hour (normal range, 0 to 30 mm/hour) and C-reactive protein was 9.4 g/dL (normal value, less than 1 mg/dL). Urine screening toxicology was negative and gastric secretions were obtained for further toxicology. Blood, stool, gastric, and urine cultures remained negative. Examination
JAAPA Journal of the American Academy of Physician Assistants
Copyright © 2014 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
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29
CASE REPORT
Key points The classic presentation for botulism includes progressive brainstem dysfunction and symmetric descending paralysis of all extremities; patients are at risk for respiratory failure. Importantly, patient alertness remains intact. The differential diagnosis includes Guillain-Barré syndrome, myasthenia gravis, brainstem stroke, polyradiculitis, intoxication, and acute (brainstem) encephalitis. Nerve conduction studies and EMGs are helpful in rapidly differentiating this disorder from other diseases. Early empiric therapy with botulism antitoxin is needed to stop this otherwise invariably progressive disease. Recovery in a patient with pronounced deficits is often guarded.
of the cerebrospinal fluid (CSF) showed no white or red blood cells, normal protein of 50 mg/dL, and normal glucose of 78 mg/dL. Gram stain and CSF cultures remained negative. Blood samples for lead, arsenic, and mercury exposures were negative. Autoantibodies against myelin-associated proteins (GM1/GD1a, b/Gq1b) were negative. Radiological studies included a normal-appearing chest radiograph and a brain MRI without contrast, which revealed small, multifocal signal abnormalities on diffusion and apparent diffusion coefficient weighted imaging consistent with postcardiac arrest hypoxemia-hypoperfusion injury. Nerve conduction studies and an electromyogram (EMG) were performed to delineate whether the acute weakness was induced primarily by • an efferent (motor) nerve disease such as acute motor neuropathy • a problem at the junction of the motor nerve and the muscle membrane (faulty muscle endplate transmission such as in myasthenia gravis) • an intrinsic muscle illness, such as acute myositis. Nerve conductions, both sensory and motor, were completely within normal limits in all extremities. However, stimulation of motor nerves evoked was consistent with either a problem of electric communication between the nerve and muscle (endplate) or intrinsic muscle illness. However, subsequent EMGs showed no signs identifying intrinsic muscle disease; therefore, the severe weakness in this patient was attributable to a primary problem of the motor endplates. Acute failure of motor endplate function can only be due to a distinct group of illnesses, among them myasthenia gravis and botulinum toxin exposure (Table 1). Empiric antitoxin therapy against botulism was immediately started. On day 7 of admission, we received from the CDC a report of positive titers of botulism type A toxin in this patient’s gastric fluid. A concomitantly obtained initial mouse bioassay remained negative; however, a second gastric sample treated with heat shock to promote spore germination 30
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killed the test animal. Antitoxin substudies identified that only antitoxin A but not antitoxin E was protective against this toxin-producing Clostridium strain. DISCUSSION About 110 cases of botulism are reported each year in the United States. Botulism is a neuroparalytic illness caused by a potent toxin produced by Clostridium botulinum. The toxin is broken down into seven immunologically different types (A through G), but only four (A, B, E, and rarely F) are known to cause human disease.1 Depending on the mode of toxin acquisition, five forms of botulism are differentiated. • Foodborne botulism results from the ingestion of food containing preformed toxin. With the help of the local health department, the patient’s home was searched for suspicious food that may have been contaminated. The patient’s botulism was traced to improperly stored food containing preformed toxin. • Wound botulism is caused by organisms that multiply and produce toxin in a contaminated wound. • Infant botulism is due to the production of toxin by germinating spores of C. botulinum in the infant’s intestine. Infants can develop botulism by ingesting substances that contain spores, such as dirt, dust, and contaminated honey. • Enteric infectious botulism occurs when the patient has no evidence of wound botulism and no food vehicle is identified. • Inhaled botulism is caused by aerosolized toxin released in an act of bioterrorism.2 In our patient, botulinum type A toxin was found in the serum specimen taken before antitoxin administration. In addition, samples of jarred food at his house, including a hot sauce from the Dominican Republic, underwent ELISA testing that was consistent with botulinum toxin type E. The positive test could be explained by cross-reactivity between types A and E, explaining this subtype difference. We could not determine whether he acquired the infection via food or became infected secondary to intestinal colonization (type A spores are ubiquitous in nature and can be found in the GI tract of asymptomatic hosts). During his hospitalization, the patient required tracheotomy and percutaneous endoscopic gastrostomy for persistence of oropharyngeal dysfunction. He also received a course of trimethoprim/sulfamethoxazole DS for Haemophilus influenzae pneumonia. Weaning the patient from the ventilator was unsuccessful even after tracheotomy. To control musculoskeletal and neuropathic pain, he received a fentanyl patch and pregabalin. At the time of discharge 4 weeks later, the patient had modestly improved. He was awake for most of the daytime, but unable to open his eyes voluntarily. He used hand squeezing signals to reply yes or no to questions. His oculomotor nerve palsy remained unchanged, but his pupils became light-sensitive. He could not protrude his tongue, but started to minimally purse Volume 27 • Number 8 • August 2014
Copyright © 2014 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
A 59-year-old man with acute onset of paralysis TABLE 1. Diagnostic
features of GBS, myasthenia gravis, and botulism GBS
Myasthenia gravis
Botulism
Antibody formation against peripheral nerves myelin and/or axons
Antibodies against acetylcholine receptors
Endotoxin inhibits acetylcholine release
Eyes
Ptosis; fixed and dilated pupils (rare)
Ptosis, normal pupils
Fixed, dilated pupils
Reflexes
Absent
Present
Absent
Weakness pattern
Ascending, symmetrical; facial muscles may be involved
Muscle fatigue; may include cranial and external eye muscles
Descending paralysis; often early involvement of pupillary muscles
Autonomic dysfunction Common
Seen as medication adverse reaction
Common
Muscle fatigability
No
Yes
No
Respiratory failure
Yes with advanced disease
Yes with advanced disease
Often and early
Course
Acute and subacute
Subacute and relapsing
Acute
CSF
Increased protein
Normal
Normal
Specific antibodies
Anti-GQ1b; anti-GD1a; anti-GM1; anti-GD3
Anti-AChR; anti-MuSK; antistriated muscle; antistriational
Anti-C. botulinum (A-F) toxoid
EMG/nerve conduction
Abnormal EMG predominantly showing denervation; nerve conduction usually delayed
Abnormal EMG with signs of decrease responses (fatigue) with high-frequency repetitive stimulation tests; normal nerve conduction studies
Abnormal EMG with pronounced increased responses with rapid repetitive nerve stimulation; conduction studies normal
Treatment
Plasmapheresis, IVIG, corticosteroids
Plasmapheresis, IVIG, corticosteroids
Antitoxin, wound debridement, remove contaminated food source
Injury mechanism Exam features
Key diagnostic findings
his lips and had a positive gag reflex. The patient’s upper extremities were flaccid proximally with gradual distal improvements of strength to 3/5 wrist and finger flexion and extension. His lower extremity strength was 0/5 in both the hamstrings and knee extension and flexion; his foot dorsiflexion and plantar flexion had improved to 4+/5 and 2/5, respectively. He continued to be areflexic with mute toes and flaccid muscle tone. He remained ventilator dependent on synchronized intermittent mandatory ventilation at 40% Fio2. The patient continued to have a complicated course after his initial hospital stay. While in a long-term care facility, he developed a stage IV sacral ulcer that subsequently developed into osteomyelitis and frank sepsis, requiring intensive hemodynamic and cardiac resuscitation. One year after being diagnosed with botulism, he remained unaware of his cardiac arrest, but otherwise had normal wakefulness, orientation, memory, and cognition. However, his marked extremity weakness (2-3 out of 5 muscle strength) persisted, as did his ventilator dependency. This patient’s case illustrates the importance of early recognition of the classic triad of botulism: clear mentation, bulbar palsy, and symmetric descending paralysis in an afebrile patient with acute symptom onset.3 Botulism characteristically begins with paralysis of the cranial motor nerves, leading to ocular and pupillary palsies and bifacial
weakness. Almost simultaneously, ongoing dropout of skeletal muscle nerve fibers leads to descending paralysis noted by the patients and clinicians as proximal and later distal extremity weakness. The muscle weakness progresses quickly to complete plegia of all extremity muscles with accompanying respiratory failure and, if not treated promptly, the risk for hypercapnic hypoxemic arrest, as in our patient.4 Notably, patients are fully alert during the progressive illness and are aware of their increasing deficits. This important fact needs to be taken into account when caring for and interacting with patients suffering from botulism. Adjunctive therapy to control pain, anxiety, and depression is frequently needed. As in our patient, motor strength recovery is generally slow and often incomplete, taking anywhere from weeks to several months, and persistent deficits are common.1 JAAPA REFERENCES 1. Shapiro RL, Hatheway C, Swerdlow DL. Botulism in the United States: a clinical and epidemiologic review. Ann Intern Med. 1998;129(3):221-228. 2. Sobel J. Botulism. Clin Infect Dis. 2005;41(8):1167-1173. 3. Badhey H, Cleri DJ, D’Amato RF, et al. Two fatal cases of type E adult food-borne botulism with early symptoms and terminal neurologic signs. J Clin Microbiol. 1986;23(3):616-618. 4. Hughes JM, Blumenthal JR, Merson MH, et al. Clinical features of types A and B food-borne botulism. Ann Intern Med. 1981; 95(4):442-445.
JAAPA Journal of the American Academy of Physician Assistants
Copyright © 2014 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
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31
A 59-year-old man with acute onset of paralysis Richard S. Cassa, MPAS, PA-C; Axel J. Rosengart, MD, PhD, MPH
CASE A 59-year-old man presented to the ED complaining of “not feeling right” and “a thick throat.” Upon awakening that morning, he had experienced subacute onset of slurred speech, upper airway swelling, and ascending weakness of all extremities. The symptoms worsened progressively over the next 6 hours, prompting him to go to the ED. History The patient lived independently and had a history of schizoaffective disorder and hypertension. He was taking venlafaxine, risperidone, hydroxyzine, aspirin, pravastatin, and hydrochlorothiazide at home. Two weeks before this admission, the patient had lost his job as a store attendant and since then had been unable to obtain medication refills. After stopping his medication, the patient became increasingly withdrawn and inattentive to his home environment and personal hygiene. He was unable to leave his home and perform his activities of daily living. Also, he did not act on the fact that his refrigerator—filled with perishable imported food—was not working properly. In the ED, the patient was afebrile with a BP of 89/65, heart rate of 86, respirations of 32 and labored, and oxygen saturation of 91% on 2 L of supplemental oxygen via nasal cannula. Over the next 2 hours, his respiratory function declined sharply, leading first to respiratory failure requiring endotracheal intubation and mechanical ventilation, Richard S. Cassa is a chief PA in the Department of Neurology, Division of Acute Neurosciences at New York Presbyterian Hospital-Cornell in New York City. Axel J. Rosengart is director of neurocritical care and an associate professor of neurology, neuroscience, and neurosurgery at Weill Cornell Medical College in New York City.The authors have disclosed no potential conflicts of interest, financial or otherwise. DOI: 10.1097/01.JAA.0000450805.98459.e6 Copyright © 2014 American Academy of Physician Assistants
© DR. GARY GAUGLER / SCIENCE SOURCE
ABSTRACT Botulism is a neuroparalytic illness resulting from the action of a potent toxin produced by the organism Clostridium botulinum. It can present with a classic triad of clear mentation, bulbar palsy and symmetric descending paralysis. Treatment is symptomatic and includes a botulinum antitoxin. Keywords: Clostridium botulinum, Guillain-Barré syndrome, myasthenia gravis, botulism, schizoaffective disorder, paralysis
FIGURE 1. Color-enhanced scanning electron micrograph of
C. botulinum, which causes botulism
then cardiac arrest. An examination after resuscitation showed a hemodynamically and respiratory stabilized patient who was unable to open his eyes; had bilateral fixed, dilated pupils; and severe weakness of all extremities. A CT scan of the head was unrevealing. The patient was subsequently transferred to our center for further care. On arrival at our hospital, the patient was awake and alert but unable to open his eyes. He was still mechanically ventilated. He responded appropriately to yes/no questions with hand grasping, revealing full orientation and no deficits in key cognitive areas. His pupils were 5 mm, unreactive, and isocoric; he had bilateral complete ophthalmoplegia with absent oculocephalic, corneal, and gag reflexes. A motor examination identified severe proximal 1/5 and distal 3/5 symmetric weakness of all extremities with normal muscle bulge and tone but absent reflexes and no Babinski signs. Sensation was intact to all modalities. He had no skin lesions. Cardiorespiratory and abdominal examinations were within normal limits. Routine blood work was normal, including liver function tests and thyroid panel. The patient’s erythrocyte sedimentation rate was 14 mm/hour (normal range, 0 to 30 mm/hour) and C-reactive protein was 9.4 g/dL (normal value, less than 1 mg/dL). Urine screening toxicology was negative and gastric secretions were obtained for further toxicology. Blood, stool, gastric, and urine cultures remained negative. Examination
JAAPA Journal of the American Academy of Physician Assistants
Copyright © 2014 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
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29
CASE REPORT
Key points The classic presentation for botulism includes progressive brainstem dysfunction and symmetric descending paralysis of all extremities; patients are at risk for respiratory failure. Importantly, patient alertness remains intact. The differential diagnosis includes Guillain-Barré syndrome, myasthenia gravis, brainstem stroke, polyradiculitis, intoxication, and acute (brainstem) encephalitis. Nerve conduction studies and EMGs are helpful in rapidly differentiating this disorder from other diseases. Early empiric therapy with botulism antitoxin is needed to stop this otherwise invariably progressive disease. Recovery in a patient with pronounced deficits is often guarded.
of the cerebrospinal fluid (CSF) showed no white or red blood cells, normal protein of 50 mg/dL, and normal glucose of 78 mg/dL. Gram stain and CSF cultures remained negative. Blood samples for lead, arsenic, and mercury exposures were negative. Autoantibodies against myelin-associated proteins (GM1/GD1a, b/Gq1b) were negative. Radiological studies included a normal-appearing chest radiograph and a brain MRI without contrast, which revealed small, multifocal signal abnormalities on diffusion and apparent diffusion coefficient weighted imaging consistent with postcardiac arrest hypoxemia-hypoperfusion injury. Nerve conduction studies and an electromyogram (EMG) were performed to delineate whether the acute weakness was induced primarily by • an efferent (motor) nerve disease such as acute motor neuropathy • a problem at the junction of the motor nerve and the muscle membrane (faulty muscle endplate transmission such as in myasthenia gravis) • an intrinsic muscle illness, such as acute myositis. Nerve conductions, both sensory and motor, were completely within normal limits in all extremities. However, stimulation of motor nerves evoked was consistent with either a problem of electric communication between the nerve and muscle (endplate) or intrinsic muscle illness. However, subsequent EMGs showed no signs identifying intrinsic muscle disease; therefore, the severe weakness in this patient was attributable to a primary problem of the motor endplates. Acute failure of motor endplate function can only be due to a distinct group of illnesses, among them myasthenia gravis and botulinum toxin exposure (Table 1). Empiric antitoxin therapy against botulism was immediately started. On day 7 of admission, we received from the CDC a report of positive titers of botulism type A toxin in this patient’s gastric fluid. A concomitantly obtained initial mouse bioassay remained negative; however, a second gastric sample treated with heat shock to promote spore germination 30
www.JAAPA.com
killed the test animal. Antitoxin substudies identified that only antitoxin A but not antitoxin E was protective against this toxin-producing Clostridium strain. DISCUSSION About 110 cases of botulism are reported each year in the United States. Botulism is a neuroparalytic illness caused by a potent toxin produced by Clostridium botulinum. The toxin is broken down into seven immunologically different types (A through G), but only four (A, B, E, and rarely F) are known to cause human disease.1 Depending on the mode of toxin acquisition, five forms of botulism are differentiated. • Foodborne botulism results from the ingestion of food containing preformed toxin. With the help of the local health department, the patient’s home was searched for suspicious food that may have been contaminated. The patient’s botulism was traced to improperly stored food containing preformed toxin. • Wound botulism is caused by organisms that multiply and produce toxin in a contaminated wound. • Infant botulism is due to the production of toxin by germinating spores of C. botulinum in the infant’s intestine. Infants can develop botulism by ingesting substances that contain spores, such as dirt, dust, and contaminated honey. • Enteric infectious botulism occurs when the patient has no evidence of wound botulism and no food vehicle is identified. • Inhaled botulism is caused by aerosolized toxin released in an act of bioterrorism.2 In our patient, botulinum type A toxin was found in the serum specimen taken before antitoxin administration. In addition, samples of jarred food at his house, including a hot sauce from the Dominican Republic, underwent ELISA testing that was consistent with botulinum toxin type E. The positive test could be explained by cross-reactivity between types A and E, explaining this subtype difference. We could not determine whether he acquired the infection via food or became infected secondary to intestinal colonization (type A spores are ubiquitous in nature and can be found in the GI tract of asymptomatic hosts). During his hospitalization, the patient required tracheotomy and percutaneous endoscopic gastrostomy for persistence of oropharyngeal dysfunction. He also received a course of trimethoprim/sulfamethoxazole DS for Haemophilus influenzae pneumonia. Weaning the patient from the ventilator was unsuccessful even after tracheotomy. To control musculoskeletal and neuropathic pain, he received a fentanyl patch and pregabalin. At the time of discharge 4 weeks later, the patient had modestly improved. He was awake for most of the daytime, but unable to open his eyes voluntarily. He used hand squeezing signals to reply yes or no to questions. His oculomotor nerve palsy remained unchanged, but his pupils became light-sensitive. He could not protrude his tongue, but started to minimally purse Volume 27 • Number 8 • August 2014
Copyright © 2014 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
A 59-year-old man with acute onset of paralysis TABLE 1. Diagnostic
features of GBS, myasthenia gravis, and botulism GBS
Myasthenia gravis
Botulism
Antibody formation against peripheral nerves myelin and/or axons
Antibodies against acetylcholine receptors
Endotoxin inhibits acetylcholine release
Eyes
Ptosis; fixed and dilated pupils (rare)
Ptosis, normal pupils
Fixed, dilated pupils
Reflexes
Absent
Present
Absent
Weakness pattern
Ascending, symmetrical; facial muscles may be involved
Muscle fatigue; may include cranial and external eye muscles
Descending paralysis; often early involvement of pupillary muscles
Autonomic dysfunction Common
Seen as medication adverse reaction
Common
Muscle fatigability
No
Yes
No
Respiratory failure
Yes with advanced disease
Yes with advanced disease
Often and early
Course
Acute and subacute
Subacute and relapsing
Acute
CSF
Increased protein
Normal
Normal
Specific antibodies
Anti-GQ1b; anti-GD1a; anti-GM1; anti-GD3
Anti-AChR; anti-MuSK; antistriated muscle; antistriational
Anti-C. botulinum (A-F) toxoid
EMG/nerve conduction
Abnormal EMG predominantly showing denervation; nerve conduction usually delayed
Abnormal EMG with signs of decrease responses (fatigue) with high-frequency repetitive stimulation tests; normal nerve conduction studies
Abnormal EMG with pronounced increased responses with rapid repetitive nerve stimulation; conduction studies normal
Treatment
Plasmapheresis, IVIG, corticosteroids
Plasmapheresis, IVIG, corticosteroids
Antitoxin, wound debridement, remove contaminated food source
Injury mechanism Exam features
Key diagnostic findings
his lips and had a positive gag reflex. The patient’s upper extremities were flaccid proximally with gradual distal improvements of strength to 3/5 wrist and finger flexion and extension. His lower extremity strength was 0/5 in both the hamstrings and knee extension and flexion; his foot dorsiflexion and plantar flexion had improved to 4+/5 and 2/5, respectively. He continued to be areflexic with mute toes and flaccid muscle tone. He remained ventilator dependent on synchronized intermittent mandatory ventilation at 40% Fio2. The patient continued to have a complicated course after his initial hospital stay. While in a long-term care facility, he developed a stage IV sacral ulcer that subsequently developed into osteomyelitis and frank sepsis, requiring intensive hemodynamic and cardiac resuscitation. One year after being diagnosed with botulism, he remained unaware of his cardiac arrest, but otherwise had normal wakefulness, orientation, memory, and cognition. However, his marked extremity weakness (2-3 out of 5 muscle strength) persisted, as did his ventilator dependency. This patient’s case illustrates the importance of early recognition of the classic triad of botulism: clear mentation, bulbar palsy, and symmetric descending paralysis in an afebrile patient with acute symptom onset.3 Botulism characteristically begins with paralysis of the cranial motor nerves, leading to ocular and pupillary palsies and bifacial
weakness. Almost simultaneously, ongoing dropout of skeletal muscle nerve fibers leads to descending paralysis noted by the patients and clinicians as proximal and later distal extremity weakness. The muscle weakness progresses quickly to complete plegia of all extremity muscles with accompanying respiratory failure and, if not treated promptly, the risk for hypercapnic hypoxemic arrest, as in our patient.4 Notably, patients are fully alert during the progressive illness and are aware of their increasing deficits. This important fact needs to be taken into account when caring for and interacting with patients suffering from botulism. Adjunctive therapy to control pain, anxiety, and depression is frequently needed. As in our patient, motor strength recovery is generally slow and often incomplete, taking anywhere from weeks to several months, and persistent deficits are common.1 JAAPA REFERENCES 1. Shapiro RL, Hatheway C, Swerdlow DL. Botulism in the United States: a clinical and epidemiologic review. Ann Intern Med. 1998;129(3):221-228. 2. Sobel J. Botulism. Clin Infect Dis. 2005;41(8):1167-1173. 3. Badhey H, Cleri DJ, D’Amato RF, et al. Two fatal cases of type E adult food-borne botulism with early symptoms and terminal neurologic signs. J Clin Microbiol. 1986;23(3):616-618. 4. Hughes JM, Blumenthal JR, Merson MH, et al. Clinical features of types A and B food-borne botulism. Ann Intern Med. 1981; 95(4):442-445.
JAAPA Journal of the American Academy of Physician Assistants
Copyright © 2014 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
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31
