One of the major duties of a physiatrist attending on an inpatient rehabilitation unit is the prevention and management of medical complications. Physiatrists may find this a daunting task because severely disabled patients requiring hospitalization for acute rehabilitation frequently suffer from many comorbidities. Most of these arise from the multiple-organ-system complications of prolonged immobility. Additionally, physiatrists are increasingly under pressure to decrease readmission rates to the acute care hospital.

Prevention of morbidity and mortality in the rehabilitation unit requires the implementation of basic patient safety principles. First and foremost among these principles is teamwork and communication, a skill for which rehabilitation professionals hold much pride. However, the communication skills around medical urgencies may be unfamiliar to some in the rehabilitation setting. It behooves the medical director to ensure that all staff has been trained in communication tools such as SBAR (situation, background, assessment, response).¹

Infection control is critical, and this includes close monitoring and enforcement of proper hand hygiene. Rehabilitation units should implement protocols to standardize admission orders to ensure that proper preventative measures are taken (e.g., prophylaxis for venous thromboembolism). Medication reconciliation on discharge can prevent rehospitalizations.² Lastly, rehabilitation programs should monitor quality improvement through a dashboard.³

This chapter outlines major complications and provides recommendations for prevention, diagnosis, and treatment, as well as a list of relevant therapy precautions.

Background

The prevalence of venous thromboembolism (VTE) is approximately 0.2% within the general population; however, the incidence of detected and undetected VTE varies widely.⁴ The prevalence of VTE increases markedly in patients recovering from stroke, major orthopedic or general surgery, spinal cord injury (SCI), or other major trauma and incapacitating medical illnesses. Pulmonary embolism (PE) occurs in 26% to 67% of patients with untreated proximal deep vein thromboses (DVTs), with a mortality rate of 11% to 23%.⁵ The economic burden/direct cost of VTE in the United States is estimated to be $3 billion to $4 billion annually, which does not reflect additional indirect costs of lost workdays and productivity.⁵ Use of guideline-driven VTE prophylaxis can reduce the incidence of VTE in rehabilitation patients sixfold.⁶

Prevention

Preventing DVT/VTE in the rehabilitation unit depends on the primary diagnosis (Table 53–1). The recommendations in Table 53–1 are based on American College of Chest Physician Guidelines.⁷

Diagnosis

Monitor for signs/symptoms, including swelling, tenderness, pitting edema, dilated superficial veins, fever, and erythema. Wells et al described a clinical prediction rule that is useful in determining the need for diagnostic testing.⁸ Imaging via venous ultrasound is the “gold standard” for DVT. Computerized tomographic (CT) angiography of the chest is the preferred study for PE in patients with normal renal function; in patients with renal impairment, ventilation-perfusion (VQ) scans are preferred.⁹

Treatment

Treatment consists of low-molecular-weight heparin (LMWH; enoxaparin sodium) 1.0 mg/kg bid or 1.5 mg/kg qd; the unfractionated heparin (UFH) dose is adjusted to maintain an activated partial thromboplastin time (aPTT) of 46 to 70 seconds. For warfarin or vitamin K antagonists, the goal is to maintain an international normalized ratio (INR) of between 2.0 and 3.0. The duration of treatment may vary. Vitamin K antagonists (VKAs) are recommended for 3 to 6 months in patients who have a first episode of VTE with transient risk factors, e.g., surgery, acute injury, pregnancy. Rivaroxaban is an alternative. Patients who have a first episode of VTE with concurrent cancer are recommended to be managed with LMWH for first 3 to 6 months and then VKAs until the cancer resolves. For patients with a first episode of idiopathic VTE without identifiable cause, VKAs for 6 to 12 months (consider indefinite treatment) are recommended. Patients with prothrombotic genotype (e.g., protein S, protein C, and antithrombin deficiency) who have a first episode VTE may be managed with a VKA if more than one hypercoagulable state exists. Patients with recurrent VTE are recommended to be managed with VKAs.^5,10

Therapy Precautions

Risk of embolization of DVT is thought to be greatest soon after it forms, when it is loosely attached to the vessel wall. Despite this fact, prolonged bedrest following the diagnosis of DVT/VTE is no longer recommended by recent guidelines.⁵ Therapies may be resumed 4 to 6 hours after the initial/loading dose of anticoagulant. Conversely, therapies should be deferred in patients who are substantially over-anticoagulated until the problem has been corrected (falls in this population may be catastrophic).

Background

Health care–associated pneumonia (HCAP) accounts for 1% of all hospital admissions and has a high mortality rate, estimated at 18% for hospitalized patients.^11,12 Aspiration pneumonia has a variable prevalence (22%–71%) and often is associated with comorbidities. Approximately 5% to 15% of hospitalized pneumonias are due to aspiration.^13,14 Atelectasis appears in about 90% of all anesthetized patients. with reports of 15% to 20% lung collapse at the bases.¹⁵

Prevention

All at-risk patients should receive pneumococcal and influenza vaccinations. Strategies to prevent pneumonia include avoiding intubation, if possible, minimizing sedation, improving and maintaining physical conditioning, minimizing pooling of secretions above endotracheal (ET) tube cuffs (if the patient is intubated), maintenance of ventilator circuits, and head of bed elevation. Aspiration can be prevented through dietary modifications, routine oral care, post–pyloric tube feedings, head of bed elevation, swallowing rehabilitation, and use of gastroprokinetic agents (e.g., mosapride).¹⁴ Atelectasis prevention includes implementation of chest physiotherapy, incentive spirometry, and deep breathing exercises.¹⁶

Diagnosis

Pneumonia is diagnosed by the presence of a new or progressive radiographic infiltrate plus at least two of the three following clinical features: fever > 38ºC, leukocytosis or leukopenia, and purulent secretions. This represents a clinically relevant combination of criteria for starting empirical antimicrobial therapy. Blood work (i.e., complete blood count [CBC]) and blood and sputum cultures are recommended.^11,12 Diagnosing aspiration pneumonia requires evidence of a new chest radiograph infiltrate in a dependent pulmonary segment of a patient with risk factors for aspiration.

Treatment

Antibiotics are the mainstay of therapy. Cultured specimens and sensitivities are of critical importance in identifying a causative organism. Empirical antibiotic therapy should be started as soon as possible after diagnosis (within 4 hours), but only after culture collection. Antibiotics should be tailored based on culture and sensitivity results. Antibiotics are often in accordance with local hospital policy and based on available formulary medications. A 7-day course of antibiotics is as effective as a 10-day course as long as the organism is not a nonfermenting gram-negative bacillus.¹⁷

Therapy Precautions

Frequent pulse oximetry measurements should be performed to ensure adequate oxygenation. For patients on enteral feeding, heads should be kept upright so as to prevent aspiration. Infection policies should be implemented based on causative organism and hospital policies/guidelines.

Background

Arrhythmias are common among patients in the rehabilitation unit, with atrial arrhythmias making up the majority.¹⁸ Atrial fibrillation/flutter (AF) is by far the most common atrial arrhythmia managed in the rehabilitation unit. AF affects more than 2.2 million persons in the United States and is strongly age dependent, affecting 4% of individuals older than 60 years of age and 8% of individuals older than 80 years of age.¹⁹ Premature ventricular contractions (PVCs) also occur frequently and can occur in patients with or without heart disease. Sinus bradycardia is usually chronic in nature, but acute or symptomatic sinus bradycardia is a manifestation of new myocardial infarction or heart failure and should warrant further workup (e.g., electrocardiogram [ECG], lab work, and cardiology consultation). Although not often seen in the rehabilitation unit, the current annual incidence of sudden cardiac death in the United States is estimated to be between 180,000 and 250,000 per year, mostly due to ventricular fibrillation (VF) and ventricular tachycardia (VT).²⁰

Prevention

Although patients typically are admitted to the rehabilitation unit with medications that control the heart rate, the rehabilitation team should be prudent about cardiac monitoring and identifying any cardiac changes and symptoms. Identification of medications that can alter heart rhythm (e.g., antipsychotics, antibiotics) or electrolyte levels (e.g., diuretics) is crucial. Frequent lab draws may be necessary, including monitoring of potassium and magnesium levels. Other factors to consider that may alter heart rate and rhythm include pain and hydration status.

Diagnosis

Resting 12-lead ECG, exercise testing, imaging (nuclear perfusion, magnetic resonance imaging [MRI], cardiac CT), pharmacologic stress testing, ambulatory electrocardiography (event monitor), implantable recorders, echocardiography, radionuclide angiography, coronary angiography, and electrophysiologic testing with intracardiac recording are all used for diagnosis.²¹

Treatment

Acute management of unstable arrhythmias should follow advanced cardiovascular life support (ACLS) defined protocols. Nondrug therapy includes implantable cardioverter-defibrillators (ICDs), wearable automatic defibrillators, electrolyte management (i.e., potassium, magnesium), surgery (resection of arrhythmogenic focus, ablation, cardiac sympathectomy, aneurysm resection), and surgical or percutaneous coronary revascularization.

Therapy Precautions

Therapy should be avoided in patients with accompanying symptoms. Ideally, exercise heart rate parameters are set by ECG stress testing. In the absence of these data, heart rate parameters in general should be maintained less than 65% maximum heart rate for high-risk patients and less than 80% in others.²²

Background

Delirium affects 11% to 42% of medically ill patients and complicates 24% to 89% of hospitalizations for elderly patients. The prevalence of delirium among the general population ranges from 0.5% to 13%. Approximately 9% to 28% of patients experience delirium, with up to 36% following emergent hip surgery and around 71% of patients with sepsis. The economic burden of delirium to the US health care system is more than $60,000 per patient per year.^23–25

Prevention

Early identification of patients at risk is crucial. Early initiation of management strategies in at-risk patients (i.e., environmental controls) is important for preventing delirium. It is advisable to avoid the use of physical restraints, constipation, central nervous system (CNS) activating medications (e.g., anticholinergics, antihistamines, benzodiazepines, narcotics, etc.), and catheters when possible.^23,24,26,27 Further preventive strategies include maintaining good nutrition, providing feeding/fluid assistance as needed, and using aids to improve orientation and provide frequent orientations. Provision of family photographs, clocks, calendars, and windows with outside views and verbally reorienting patients may mitigate confusion that results from disorientation in unfamiliar environments. Nursing and medical procedures, including the administration of medications, should be avoided during sleeping hours, when possible. Nighttime noise should be reduced. Staff continuity, early mobilization, adequate pain management, and the use of aids to improve vision/hearing are critical for preventing delirium.^23,24,26,27 Pharmacologic sleep agents also can be used, with haloperidol and quetiapine as the preferred agents. Due to severe side effects, antipsychotics are typically avoided in the elderly population.^23,24

Diagnosis

Acute delirium is defined as onset of confusion, inattention, or disorganized thinking/behavior over hours to days. Other features include loss of consciousness (LOC) that fluctuates during the course of the day and disturbances of perception or disturbances of the sleep/wake cycle. It is recommended to use Diagnostic and Statistical Manual (DSM) criteria to diagnose delirium using the Global Attentiveness Rating (GAR) scale or similar assessment tool.^23,24,27

Treatment

First-line treatment includes treating the underlying medical condition, along with a complete medication review to identify any delirium-causing pharmacologic agents.^23,24,26,27 Second-line treatment includes an array of pharmacologic modalities aimed at preventing patients from endangering themselves or others and controlling agitation or hallucinations. Haloperidol and quetiapine are the preferred antipsychotics, but great care should be taken in administering these medication in patients with a history of brain injury.²⁶ Other antipsychotics, including olanzapine, risperidone, and aripiprazole, are not typically recommended in the elderly population due to severe side effects. Cholinesterase inhibitors have also been used (e.g., donepezil, rivastigmine), but strong evidence is lacking in the literature. Other agents that may be employed include gabapentin and the benzodiazepines for delirium tremens only because they may exacerbate delirium.^24,27

Therapy Precautions

Environmental modifications and pharmacologic interventions, as noted earlier, should be provided.

Background

Seizures affect 0.5% to 1% of the US population with an estimated incidence of 50 new cases per 100,000 persons per year.²⁸ In the rehabilitation unit, providers may encounter patients who have suffered traumatic brain injuries (TBIs). These patients may be more prone to seizures and should be adequately monitored. The prevalence of seizures in hospitalized TBI patients is 10%, with the epileptic focus occurring in the area of the injury or scar. Most seizures occur in the first several days or weeks after TBI, but some may occur months afterwards. Most patients (70%–80%) with TBI-related seizures have some response to seizure medication and can return to most activities.²⁹

Prevention

In general, providers should avoid medications that decrease the seizure threshold or lower the efficacy of antiseizure medications. Electrolytes (e.g., calcium, magnesium) should also be monitored. Studies with antiepileptic drugs (e.g., phenytoin, phenobarbital, their combination, carbamazepine, valproate, or magnesium) in posttraumatic seizures have been marred by small sample sizes, and the evidence has been inconclusive. For most of the regimens tested, the best estimate of effect is under 25% reduction in posttraumatic seizures, well less than the 50% reduction most studies were designed to detect.³⁰ Levetiracetam has demonstrated comparable efficacy to phenytoin for posttraumatic seizure (PTS) prophylaxis and has been shown to have fewer adverse effects and monitoring considerations. The Brain Trauma Foundation recommends using phenytoin for early PTS prophylaxis.³¹

Diagnosis

History, physical examination, and seizure classification are of paramount importance. Workup includes CBC, comprehensive metabolic panel, creatine phosphokinase (CPK), lactate dehydrogenase (LDH), arterial blood gases (ABGs; pCO₂), ammonia levels, electroencephalogram (EEG), and ECG. Consider lumbar puncture (LP) if an infectious etiology is suspected. Focal neurologic signs warrant immediate neuroimaging (CT scan, MRI).³²

Treatment

Pharmacologic intervention is recommended only after two documented seizures, except if the patient is having status epilepticus.³³ Generalized seizures can be managed with valproate or lamotrigine. In the acute setting of status epilepticus, immediate management should focus on airway protection and providing oxygen. Securing intravenous (IV) access with a large-bore needle followed by 50% dextrose is ideal. IV medications include lorazepam 4 mg or diazepam 10 mg (may give additional dose at 10 minutes). IV phenytoin 15 mg/kg should be administered by slow injection to prevent seizure recurrence as benzodiazepine levels drop. If seizures persist, the patient is likely to require further barbiturate or IV anesthetic (e.g., phenobarbital 10–20 mg/kg).³⁴ In all patients with TBI, PTS prophylaxis is recommended only during the first 7 days after TBI. Phenytoin has been the most extensively studied of all the antiepileptic medications for PTS prophylaxis, but levetiracetam has demonstrated relatively equal results and has been shown to have fewer adverse effects with less frequent monitoring. Still, studies have demonstrated that levetiracetam may be associated with an increased seizure tendency.³⁵

Therapy Precautions

Seizure precautions (especially for all TBI patients), including keeping the bed in a low position with side rails up and use of padded side rails, should be implemented. Aspiration precautions such as head of bed elevation may be used. Avoid situations that may be potentially dangerous. No driving for at least 3 months or per state law. Family education on seizure management is also encouraged.

Background

Stroke is the third leading cause of death in the United States. Each year there are 700,000 strokes and 160,000 stroke-related deaths.³⁶ The economic burden of strokes to the US health care system is $45 billion.³⁷ Strokes cause 3% of the world’s disability burden.³⁸ Types of stroke include ischemic (80%), intracerebral hemorrhagic (15%), and subarachnoid hemorrhagic (5%). Sources of stroke are thrombotic (50%), cardioembolic (20%), lacunar (25%), and miscellaneous (e.g., vasculitis, arterial dissection, 5%).³⁷

Prevention

Secondary prophylaxis in the inpatient rehabilitation unit relies on preventing new strokes and decreasing associated risk factors. Patients with ischemic strokes should be started on antiplatelet drugs (e.g., aspirin or clopidogrel) as well as lipid-lowering agents (e.g., statin).³⁹ Patients with embolic strokes need therapeutic anticoagulation with warfarin, typically with INR ranges between 2.0 and 3.0. Blood pressure should be normalized with appropriate antihypertensive medications. In brain stem strokes, systolic blood pressure should be maintained at a minimum level to prevent further ischemia.³⁹

Diagnosis

Diagnosing stroke in the inpatient rehabilitation unit focuses on identification of new neurologic deficits. Symptoms such as headache and altered mental status should prompt rapid assessment in stroke patients. Emergent head CT scan or MRI (along with cerebral angiography) should be ordered in patients who present with the above-mentioned clinical manifestations or in those with suspected new ischemia or hemorrhage.³⁷

Treatment

Timely recognition is crucial for reduction of stroke-related morbidity and mortality. Aspirin should be given once intracranial hemorrhage can be excluded. Dissolution of clots can be attempted with administration of IV tissue plasminogen activator (tPA) in appropriately selected patients with onset of symptoms of less than 4.5 hours.³⁷ If indicated, recanalization procedures can be done (intraarterial tPA, angioplasty, mechanical disruption of clots using specialized catheters, laser or ultrasound energy). Immediate poststroke interventions should focus on life support through respiratory and cardiac care, including blood pressure control (permissive hypertension initially), monitoring of oxygen saturation and blood glucose level, prevention of metabolic disturbance, maintenance of organ function, and management of elevated intracranial pressure. Antibiotics, antipyretics, and insulin should be used to manage infection, fever, and hyperglycemia.³⁷

Therapy Precautions

Exercise should be avoided in patients with new neurologic deficits or until elucidation of symptoms has been determined, the patient has been stabilized, and appropriate cardiac parameters have been set.

Background

Hypertension affects more than 50 million people in the United States and up to 1 billion people worldwide.⁴⁰ The incidence of hypertension increases with age and is higher in men. The incidence of hypertension is twice as high in African Americans than in Caucasians.⁴⁰ Prevalence and incidence are slightly higher in men than in women. It is estimated that approximately 1% of people with hypertension will develop a hypertensive crisis at some point in their lives.^40,41 In turn, hospitalizations for hypertensive crises have tripled in recent decades.⁴⁰ In patients with SCI, providers should monitor for symptoms and signs of autonomic dysreflexia (see Chapters 15 and 16 for details).