INTRODUCTION
As the role of physiatrists continues to evolve, the practice of rehabilitation medicine may pose additional challenges to physicians who manage patients with acute and chronic conditions that affect overall function. Medical emergencies, although infrequent, are reported in the rehabilitation setting, and staff must be trained in appropriate responses. The physiatrist must also know when to request early consultation to prevent minor medical problems from developing into major medical catastrophes. Physiatrists are frequently the “gatekeepers” of medical and nonmedical services when patients are participating in rehabilitation. The idea of gatekeeping, as promoted in other specialties such as family medicine, internal medicine, and pediatrics, requires that physiatrists be involved in the general coordination and medical care of patients with disability.
Health insurers, particularly Medicare, have continued to promote financial incentives for inpatient rehabilitation for acutely ill patients and patients with several comorbidities. Patients are admitted to an acute inpatient rehabilitation unit with the expectation that they will be able to tolerate or participate in at least 3 hours of rehabilitation services per day. The broader interpretation of the 3-hour rule supports the treatment of medical problems that previously required transfer to an acute medical floor. Acute medical events, such as deep vein thrombosis, pneumonia, chest pain, or high blood pressure, are treated in the inpatient rehabilitation unit—unless these conditions suggest hemodynamic instability—with the expectation that the patient’s progress and functional recovery may be interrupted many times during the acute rehabilitation program In addition, many managed health care providers, as well as Medicare, will not pay for hospital-based inpatient rehabilitation programs unless medical justification is explicitly defined to keep the patient in a hospital setting. Patients are expected to have active comorbidities that require medical management by a physiatrist or a consultant during their progression through functionally oriented programs, and merit a hospital-based rehabilitation stay. Otherwise, less-expensive settings for participating in rehabilitation programs are sought.
Several factors have contributed to changes in the types of patients who utilize acute rehabilitation settings, among them:
Older patients are participating in rehabilitation. More people are living beyond the age of 65 years. Aging baby boomers are becoming more involved in their health care management.
Sicker patients are participating in rehabilitation (eg, those with traumatic brain injury, spinal cord injury, and multiple traumas).
More people with chronic diseases that are treated with highly technical surgical and medical interventions are participating in rehabilitation.
Thus, changes in the overall demographic distribution, advancing medical and surgical knowledge and methods, and social policies directing cost-containment are creating a rehabilitation population at greater risk for developing medical emergencies that may interfere with traditional rehabilitation programs. Rehabilitation professionals are expected to prevent emergencies by anticipating the anatomic and pathophysiologic impact of rehabilitation interventions in such high-risk patients.
[PubMed: Publication No. 100-01]. Available at: http://www.cms.gov/Regulations-and-Guidance/Guidance/Manuals/Internet-Only-Manuals-IOMs-Items/CMS012673.html.
AUTONOMIC DYSREFLEXIA
Autonomic dysreflexia has been described as the classic rehabilitation emergency. This life-threatening condition occurs in patients with a spinal cord injury (SCI) at the level of T6 or above as a consequence of unchecked sympathetic tone. (Complications of SCI are described in detail in Chapter 12.)
Symptoms include a sudden increase in systolic blood pressure that is 20 mm Hg above baseline, pounding headache, flushing or sweating above the lesion (ie, face, neck, and shoulders), nasal congestion, blurry vision, piloerection, and meiosis. Bradycardia is classically described, although not always present, and tachycardia may even occur. In evaluating the increase in blood pressure, it is important to note that the normal systolic blood pressure for a patient with an SCI above T6 is 90–110 mm Hg. The differential diagnosis is limited and includes increased intracranial pressure, with resultant hypertension and bradycardia (particularly if the patient has a known concomitant traumatic brain injury), and pheochromocytoma.
Immediate treatment must ensue to prevent potentially life-threatening complications, such as cerebrovascular accident or intracranial hemorrhage, retinal hemorrhage, seizure, myocardial infarction, cardiac arrhythmia, and pulmonary edema.
The first step in management is to raise the head of the bed or sit the patient up, thus causing blood to pool in the lower limbs and abdomen. Next, all constricting clothing and external devices, such as compression stockings, abdominal binders, and Foley leg bags, should be removed or loosened. The key component in management is then to quickly survey the patient and alleviate any noxious stimuli below the level of the SCI. The urinary system is the most common source, stemming from bladder distention or irritation. Other considerations are fecal impaction, in-grown toenails, pain, menstruation, preeclampsia (if pregnant), and abdominal emergencies, such as appendicitis, cholecystitis, or pancreatitis.
Evaluation should begin with the urinary system. If the patient has an indwelling catheter, the entire length should be checked for the presence of kinks or obstructions, proper placement should be verified, and the tube should be flushed. If the patient does not have a Foley catheter, a straight catheter can be inserted with lidocaine jelly. Attention should then be given to the bowels and fecal impaction, although the physician can consider waiting until after medications have been given, as disimpacting with lidocaine jelly can initially worsen autonomic dysreflexia. When turning the patient to check for stool, recall that the more acute and more cephalad the injury, the greater the risk of vagal-mediated bradycardia, which can compound bradycardia associated with autonomic dysreflexia. Throughout these steps, blood pressure should be checked every 2–5 minutes until the patient is stabilized.
If the systolic blood pressure remains greater than 150 mm Hg, medications should be started while further causes are investigated. First-line treatments are nifedipine or nitroglycerin. The advantage of topical nitroglycerin, in patch or paste form, is that it can be removed if the condition resolves or blood pressure drops too low. If nitroglycerin patch or paste is used, 1–2 inches is placed above the lesion; alternately, a 0.4-mg sublingual nitroglycerin tablet may be given. Nifedipine, 10 mg, can be provided in capsule form, which can be chewed or crushed and swallowed for rapid absorption. This dose can be repeated in 30 minutes if necessary. Caution is advised when using nitroglycerin as many individuals with SCI take phosphodiesterase inhibitors for erectile dysfunction and interaction of these drugs could result in drastic hypotension. Because blood pressure tends to normalize rapidly after the inciting event of autonomic dysreflexia is removed, long-acting antihypertensive medication is not recommended as significant hypotension may ensue. β blockers should be avoided as they may cause excessive α-adrenergic activity.
Blood pressure should continue to be monitored for at least 2 hours after initial improvement. Persistence of autonomic dysreflexia necessitates transfer to an intensive care unit (ICU) or emergency department for close hemodynamic and telemetry monitoring and titration of more aggressive intravenous blood pressure medication, such as hydralazine, nitroglycerine, or nitroprusside.
SYMPATHETIC STORM IN TRAUMATIC BRAIN INJURY
Sympathetic storm describes a disturbance in autonomic control that goes by many names, with some preferring the term paroxysmal autonomic instability with dystonia (PAID). It occurs in 15–35% of patients with severe traumatic brain injury. When uncontrolled it can result in arrhythmias, myocardial infarction, neurogenic pulmonary edema, and secondary brain injury as a result of intracranial hemorrhage, increased intracranial pressure, increased temperature, or some combination of these.
Clinical manifestations may include any combination of paroxysmal episodes of tachycardia, hypertension, tachypnea, hyperpyrexia, agitation, diaphoresis, and dystonia. The differential diagnosis must initially include infection, especially when fever is a predominant feature, although other entities should be considered. These include delirium tremens, thyroid storm, neuroleptic malignant and serotonin syndromes (if causative medications have been utilized), and intrathecal baclofen withdrawal.
The management of PAID begins with an evaluation for any noxious stimuli, as described earlier in the initial treatment of autonomic dysreflexia in SCI. A calm and quiet environment should be provided. An infectious source of fever should also be sought if there has not been an extensive recent workup. Additional tests to rule out alternative diagnoses may include electrocardiography (ECG), chest radiography, thyroid panel, basic metabolic panel, and creatine kinase level.
Medication should be initiated if PAID persists despite environmental control and alleviation of potential noxious stimuli. First-line medications are propranolol or opioids, with the choice depending on the predominant symptoms. For hypertension and tachycardia, propranolol may be started at 10 mg every 12 hours and titrated up in 10-mg intervals. Oxycodone or morphine can be effective to decrease the sympathetic outflow, as well as treat unresolved pain that may be triggering the storm. Oxycodone can be given at a dosage of 5 mg every 4 hours and titrated up in 5-mg increments or, if enteral access is not possible, morphine, 2 mg intravenously, can be given every 4 hours and increased by 1 or 2 mg with successive doses.
Alternative, less frequently used medications include gabapentin and bromocriptine. Gabapentin has been found to be effective at starting dosages of 300 mg three times daily, with titration up to 600-mg doses. Caution should be used in patients with renal dysfunction (maximum dosage, 300–400 mg/day). For PAID that consists primarily of fever and diaphoresis, bromocriptine can be tried at dosages of 2.5–5 mg every 8 hours and may be titrated up to 30 or 40 mg daily. A cooling blanket or ice packs may also be helpful for patients with persistent high fevers.
SEIZURES
A primary rehabilitation diagnosis of traumatic brain injury, cerebrovascular accident, or other intracranial pathology places patients at a higher risk for seizures than the general population and is associated with more serious underlying causes of initial or breakthrough seizures, such as recurrent bleeding, infarction, and infectious foci. Uncontrolled seizures are medical emergencies that require rapid and aggressive treatment to prevent further neurologic damage and systemic complications. They can result in pronounced systemic decompensation, including respiratory failure, cardiac arrhythmias, hyperthermia, lactic acidosis, aspiration pneumonitis, and rhabdomyolysis.
Initial management must consist of closely monitoring the airway and oxygenation, checking the blood glucose level, and obtaining intravenous access. Transfer to the emergency department or ICU should be initiated while further stabilization is being carried out, as described below.
Lorazepam is the first-line medication and should be given at 2–4 mg (0.1 mg/kg) intravenously and may be repeated at 2 mg/min, up to a maximum dose of 4 mg per dose and 8 mg in 12 hours. If intravenous access is not obtainable, lorazepam may be given intramuscularly. If lorazepam is not available, a reasonable alternative is diazepam, 10 mg rectally.
If the patient is still seizing, phenytoin, 15–20 mg/kg intravenously, can be considered and repeated at 10–15 mg/kg 20 minutes later if necessary. Phenytoin should be given in a monitored setting, if possible, because of its proarrhythmic effects. Once the situation permits, several laboratory values should be obtained, including electrolytes, blood glucose, and seizure medication levels. Scheduling the patient for a computed tomography (CT) scan of the head without contrast should be considered when seizures are under better control.
FALLS
Falls are unfortunately common among patients with the functionally impairing diagnoses that require inpatient rehabilitation. Between 14% and 65% of stroke survivors experience falls while inpatients at an acute care or rehabilitation hospital. Falls in this population can result in serious injuries, such as fracture and intracranial hemorrhage. Hip fractures occur at a four times higher rate in patients with stroke than in the general population.
The management of a fall, as with all emergencies, begins with verification of hemodynamic stability. Once the patient is assured to be stable, an extremely careful history and physical examination must ensue, both for patient safety and potential medicolegal purposes. The examiner should determine if the fall was witnessed, and if so, speak directly to the witness and the patient. It is essential to document clearly what the witness and patient state has occurred, particularly regarding the mechanism of the fall, including whether the head was struck and if an alteration of consciousness occurred. Further questioning of the patient should focus on any specific complaints and should include a thorough neurologic and cardiopulmonary review of systems to help rule out a fall due to syncope or other acute medical condition. The physical examination should include evaluation for gross deformity, head laceration or hematoma, hip logroll, heel strike, and spinal step-off, as well as a complete neurologic examination, for comparison to baseline. Further attention should be paid to any area or system that has been potentially injured once hip, spine, and neurologic stability are verified.
Based on the clinical findings, imaging may be necessary. The physician should consider obtaining an emergent CT scan of the head without contrast if a change in mental status, head trauma, or an unwitnessed fall in a patient with a craniectomy has occurred. If CT scan is not indicated, it should be clearly documented that no head trauma or change in mental status has occurred. Plain radiographs of other injured body parts should be considered based on clinical suspicion of injury. Frequent neurologic checks, as often as every 1–2 hours, should be performed on any patient who hit his or her head and in whom a CT scan was performed that was negative for acute injury, or not done at all.
The focus should then be directed at preventing future falls through reinforcement of existing safety measures (eg, encouraging patients to ask for assistance with getting out of bed), as well as consideration of additional means. For example, less-aggressive physical barriers, including elevated side rails, a low bed with floor mats, and a bed-enclosure, might be appropriate, depending on the patient’s condition. Changing the room environment (eg, by minimizing the noise level or bright lights) should also be considered. If a patient continues to be at a high risk for falling or has actually repeatedly fallen, chemical or physical restraints may be necessary to prevent harm. Options include low-dose quetiapine (12.5–25 mg) or risperidone (0.5 mg) and, lastly, a Posey vest while in bed and a lap belt when in a chair for safety reasons. The occurrence of major patient events, such as a fall, should always be communicated directly to the patient’s primary contact person in a timely fashion.
ACCIDENTAL GASTROSTOMY (PEG) TUBE DISLODGEMENT
The accidental dislodgement of percutaneous endoscopic gastrostomy (PEG) tubes is estimated to occur in 1.6–20% of patients with the device. The paramount management consideration is the time from PEG placement. If a PEG tube is dislodged less than 2–4 weeks after the procedure, it should not be reinserted blindly as the gastrocutaneous stomal tract is not mature. Attempting to reinsert the tube can lead to an increased risk of separation from the abdominal wall, intraperitoneal tube insertion, and possible peritonitis from the leakage of gastric contents or tube feedings into the peritoneum. Adequate healing may require 4 weeks or longer in patients with factors that impair wound healing, such as malnourishment, steroid or other immunosuppressant therapy, and diabetes mellitus, which are not uncommon in the rehabilitation population. An additional factor is the traumatic injury often caused by a traction removal of the PEG, which increases the risk of tract disruption.
If the PEG tube is dislodged soon after insertion (ie, within 2–4 weeks), an urgent general surgery or gastroenterology consultation should be requested if available; otherwise the patient should be transferred to the emergency department or ICU as acute care may be warranted. These services may be able to facilitate image-guided tube reinsertion, although open surgical intervention or intravenous antibiotic therapy may also be necessary.
If more than 2–4 weeks have elapsed from insertion of the PEG tube to its dislodgement, reinsertion should be attempted as soon possible after the dislodgement. This will help to avoid the need for a more invasive procedure, as mature stomas may close within minutes to hours. If the PEG tube is intact, the balloon should be deflated and a gentle attempt made to reinsert the tube into a mature tract that has been lubricated with lidocaine jelly. The tube should never be forced, as a false tract or separation of the stomach from the external stoma can occur. If the initial tube is not intact or easy to reinsert, a Foley catheter (16–20 French) can be used. Once the tube is placed in the stomach, the balloon is inflated with saline and gentle traction is used to draw the balloon to the stomach wall. An urgent supine abdominal radiograph should be obtained after injecting 20–30 mL of water-soluble contrast solution (diatrizoate meglumine diatrizoate sodium [Gastrografin]) into the tube to confirm placement and rule out extravasation. Feedings should never be restarted or medications given until proper placement is confirmed. If the replacement tube is internally leaking, an emergent surgery consultation should be requested, if available.
ACCIDENTAL TRACHEOSTOMY TUBE DECANNULATION
The management of accidentally dislodged tracheostomy tubes is similar to that of PEG tubes, in that emergent nature and management vary according to the time frame after placement. Inadvertent decannulation has the potential to become life threatening, especially if it occurs before the tract between the skin and the trachea has matured.
If decannulation occurs less than 7 days after insertion, the tube should not be replaced blindly, as the stomal tract is not mature and a false passage into the mediastinum and subsequent respiratory arrest can occur. In this early time frame, the patient should be immediately ventilated using a bag–valve–mask and 100% fraction of inspired oxygen (Fio2), while pulse oximetry is continuously monitored. If available, emergent anesthesiology (and possibly ear–nose–throat or general surgery) consultation should be requested for possible reinsertion using fiberoptic guidance or orotracheal intubation. The patient should be transferred immediately to an emergency department if the preceding services are not available.
In the period between 1 week and 1 month after initial insertion, the risk of tube misplacement progressively decreases. During this time frame, the tracheostomy tube may be reinserted at the bedside using a careful and delicate technique; however, consideration should still be given to obtaining an urgent consultation for fiberoptic evaluation of placement. Once the stomal tract has matured, safe reinsertion may be accomplished without image guidance; however, oxygenation should still be closely monitored. When replacing the tube, the inner cannula is first removed, then the obturator is inserted and the cuff is deflated. Next, the tracheostomy tube is lubricated and an attempt is made to reinsert it. If minor difficulty is encountered, a smaller sized tube can be tried. If adequate ventilation cannot being provided or the patient is otherwise in distress, he or she should be transferred immediately to emergent services.
CHEST PAIN
Chest pain, pressure, or discomfort is a symptom often encountered on rehabilitation units and can occur as a result of cardiovascular, pulmonary, gastrointestinal, musculoskeletal, or psychological disorders. Life-threatening causes of chest symptoms, such as acute coronary syndrome (ACS), pericarditis, aortic dissection, pulmonary embolism (PE), pneumonia, and esophageal rupture, must first be ruled out before considering other causes. To make matters more complicated, certain patients with ACS, especially the elderly, women, and diabetics, may not present with chest complaints but with atypical symptoms such as left shoulder or back pain, dyspnea, and nausea.
Rehabilitation patients, particularly those who have experienced a stroke or amputation as a result of peripheral vascular disease, are at a higher risk of having ACS as they often have coronary artery disease as well. Recent surgery, especially orthopedic procedures, cancer, trauma, immobilization, presence of deep vein thrombosis, and hypercoagulable states, also predispose them to developing PE. They are also at high risk of pneumonia, which may manifest with chest pain, although often there are associated pulmonary symptoms. Possible causes of chest pain are included in Table 36–1.