Further Outpatient Care
The most significant improvements in ventilatory and upper airway muscle strength occur over the first few months, and, in some patients, recovery may not be complete for as long as a year. Residual symptoms such as fatigue and shortness of breath may linger for years. [41] Close follow-up is crucial.
Follow-up with other consultants, such as physical medicine and rehabilitation specialists, physical and occupational therapists, nutritionists, and psychiatrists, should be obtained as needed.
Further Inpatient Care
Neurologic Monitoring
Serial neurologic examination focusing on bulbar nerves and respiratory status should be performed with frequency of examination tailored to rapiditiy of disease progression. [1]
Respiratory Monitoring
Apart from early receipt of BAT (within 12 hours of presentation), there are no known specific signs or symptoms that suggest which patients with botulism will develop respiratory failure, therefore, respiratory monitoring can be extrapolated from management of other neuromuscular syndromes such as Guillian-Barré or Myasthenia Gravis. [42]
Patients with rising end-tidal CO2, forced vital capacity < 20 mL/kg, maximum negative inspiratory force < 30 cm H2O, and maximum expiratory pressure < 40 cm H2O may require intubation. [40]
Autonomic Nervous System Monitoring
Dysautonomia due to unopposed sympathetic nervous system stimulation is a hallmark of poisonin with toxin type B and may require cardiac and blood pressure monitoring. [1, 43]
Recovery of ventilatory and upper airway muscle strength in patients who develop respiratory failure is most significant over the first few months. The time for recovery typically ranges from 30-100 days as recovery necessitates axonal regeneration. Artificial respiratory support may be required for months in severe cases.
Transfer
Transfer is indicated if the patient's condition continues to deteriorate or if the initial hospital is unable to manage the complexities involved.
Deterrence/Prevention
Prompt notification of public health authorities regarding a suspected case of botulism may prevent further consumption of a contaminated home-canned or commercial food product.
Foodborne botulism is best prevented by strict adherence to recommended home-canning techniques. [44, 45] High-temperature pressure cooking is essential to ensure spore elimination from low-acid fruits and vegetables. Although boiling for 10 minutes kills bacteria and destroys the heat labile botulism toxin, the spores are resistant to heat and can survive boiling for 3-5 hours. Food contaminated by botulism toxins usually has a putrefactive odor; however, contaminated food may also look and taste normal. Hence, terminal heating of toxin-containing food can prevent illness and is an important preventive measure.
Wound botulism is best prevented by prompt thorough debridement of contaminated wound. [1]
Complications
Nosocomial infections
Hospital-acquired pneumonia, especially aspiration pneumonia, can occur. [4] Atelectasis and poor secretion clearance also increase the risk of hospital-acquired pneumonia. [46]
Urinary tract infection can occur from in-dwelling Foley catheters. [47]
Skin breakdown and pressure ulcer formation can occur with prolonged mobility impairment. Multiple combined interventions can be effective in their prevention. [48]
Thrombophlebitis, cellulitis, and line infections can occur. These patients often have peripheral and central intravenous catheters for prolonged periods. [49]
Fungal infections can occur; the predisposing factors include prolonged hospitalization, parenteral nutrition, and central venous catheters. [50]
DVT prophylaxis is essential to reduce the risk of these potential complications. DVT and pulmonary embolism (PE) are potential complications because patients can be bedridden for weeks to months.
Stress ulcers can occur and are common in the intensive care unit setting, espcecially in critically ill patients. Stress ulcer prophylaxis with either proton-pump inhibitor or H2 antagonist should be considered to reduce the risk of this potential complication. [51]
Other potential complications
Other potential complications include the following:
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Hypoxic tissue damage can lead to permanent neurologic deficits.
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Death
Prognosis
Botulism due to type A toxin is generally more severe than that caused by type B or E.
Mortality rates vary based on the age of the patient and the type of botulism and have significantly declined over the last century due to improvements in supportive care. The modern mortality for foodborne botulism is 5% or less. [1, 21] Wound botulism carries a mortality rate of roughly 10%. [22] The risk of death due to infant botulism is usually less than 1%. [10]
The recovery period from botulism flaccid paralysis takes weeks to months. [4] Death that occurs early in the course of disease is usually secondary to acute respiratory failure, whereas death later in the course of illness is typically secondary to complications associated with prolonged intensive care (eg, venous thromboembolism or hospital-acquired infection). Some patients demonstrate residual weakness or autonomic dysfunction for 1 year after the onset of the illness. However, most patients achieve full neurologic recovery. Permanent deficits may occur in those who sustain significant hypoxic insults.
Mortality is due to the following:
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Delayed diagnosis and respiratory failure
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Hospital complications such as nosocomial infections (usually pneumonia)
Patient Education
When preserving food at home, kill C botulinum spores by pressure cooking at 250°F (120°C) for 30 minutes. [20, 44] The toxin can be destroyed by boiling for 10 minutes or cooking at 175°F (80°C) for 30 minutes. Do not eat or taste food from bulging cans. Discard food that smells bad.
Cessation of intravenous drug use prevents wound botulism due to this vehicle.
