CAUDA EQUINA 
SYNDROME


GENERAL FEATURES


• Cauda equina syndrome (CES) is a rare illness that results from compression of the cauda equina, the bundle of nerve roots at the terminal end of the spinal cord that originates at the first or second lumbar vertebrae in most adults.


• If left untreated, CES can cause paraplegia, permanent bowel and/or bladder incontinence, and sexual dysfunction. Therefore, it should be treated as a surgical emergency. CES has no predilection for sex 
or race.
 

• CES has a variety of causes, including


– Massive central disk herniation, usually at the L5 or S1 nerve root


– Epidural hematoma


– Epidural abscess


– Subluxation from trauma


– Primary or metastatic tumor


• Lung cancer is the most common malignant cause of CES

• Clinicians should have a high index of suspicion for CES in patients with a history of malignancy and rapid progression of neurologic symptoms.


– Spinal stenosis


– Inflammatory conditions


– Iatrogenic causes


• While CES is most common in adults, children may be born with congenital spinal abnormalities or suffer trauma that results in cauda equina syndrome.


• Cauda equina syndrome manifests similarly to spinal cord compression and conus medullaris syndrome.


CLINICAL ASSESSMENT 


• History should emphasize


– Description of back pain (portrayed as different from typical back pain)


– Radiation of pain (acute or chronic)


– Neurologic deficits such as muscle weakness and paresthesia


– Bowel and/or bladder dysfunction; at initial presentation, the patient may express difficulty starting or stopping a stream of urine that is sometimes followed by incontinence of urine and then stool. Urine incontinence is caused by overflow.


– Presence of sexual impotence


• Physical examination


– Findings vary depending on 
the level and amount of compression and the area that is being 
compressed.


– Urinary retention with or without overflow incontinence is the most significant finding.


– Musculoskeletal findings include local tenderness to palpation or percussion


– Neurologic findings include loss of diminished reflexes, including bulbocavernous, patellar, and Achilles reflexes; saddle anesthesia (numbness in the perineum, genitals, buttocks, and posterosuperior thighs); decreased anal sphincter tone; bilateral lower extremity weakness; and paresthesias or sensory deficits.


DIAGNOSIS


• Initial evaluation should include plain radiographs. Although the findings may be unhelpful for confirming a diagnosis of CES, they may reveal evidence of traumatic injury, destructive lesions, or disk space narrowing.


• MRI of lumbar spine


If imaging a patient with epidural compression caused by neoplasm, obtain an MRI of the entire spine to evaluate for additional epidural metastases.


• Ultrasound revealing urinary retention greater than 500 mL, either alone or in combination with two of the following characteristics: bilateral sciatica, subjective urinary retention, or rectal incontinence symptoms, which are the most important predictors of MRI-confirmed cauda equina compressions.


TREATMENT


• The objective of treatment is to minimize progression of compression, edema, and resultant neurologic damage.


• Emergency surgical decompression of the spinal canal is recommended for definitive treatment. For patients in whom a herniated disk is the cause of CES, either a laminotomy or laminec­tomy to allow for decompression of the canal is recommended followed by gentle retraction and diskectomy. 


• Functional clinical outcome is dependent on the patient's level of disability at presentation. 


ACUTE RESPIRATORY DISTRESS SYNDROME


GENERAL FEATURES


• Acute respiratory distress syndrome (ARDS) is a severe reaction that results from direct or indirect injury to the vascular endothelium of the lung or the alveolar endothelium. ARDS causes diffuse damage to the alveoli, resulting in increased permeability of protein-rich fluid into the parenchyma of the lungs, which in turn leads to noncardiogenic pulmonary edema, poor lung compliance, and hypoxemia.


• ARDS results from an underlying condition that creates an imbalance in the proinflammatory and anti-inflammatory cytokines, leading to an exaggerated inflammatory response in the lungs.


• Sepsis is the most common cause of ARDS. Other potential etiologies include trauma, pulmonary contusion, pancreatitis, aspiration, pneumonia, burns, blood transfusions, toxic inhalations, and fat embolism.


• In the United States, there are an estimated 190,600 cases and 74,500 deaths from ARDS each year. ARDS has a substantial impact on public health with a mortality rate between 38% and 50%.


• ARDS can occur in people of all ages. Incidence increases with advanced age, reflecting the growing incidence of underlying disease in the elderly.


CLINICAL ASSESSMENT 


• The most common symptoms of ARDS include rapidly progressive dyspnea, fatigue, and cough with pink frothy sputum. Symptoms may be masked by the underlying illness that caused the ARDS.


• Physical examination findings in­clude signs of systemic inflammation, including tachypnea, tachycardia, fever, and leukocytosis.


• Other findings may include changes in mental status, severe refractory hypoxemia, hypotension, and fine crackles on auscultation of the lungs.


DIAGNOSIS


• In patients with ARDS, chest radiograph will reveal bilateral interstitial infiltrates that spare the costophrenic angles.


• The definition of ARDS established by the American-European Consensus Conference on ARDS requires the following criteria.


– Acute onset


– Bilateral infiltrates on chest radiograph


– A pulmonary artery wedge 
pressure ≤18 mm Hg or no evidence of left heart failure


– Pao₂/Fio₂ ratio ≤200 mm Hg


TREATMENT


• The goal of treatment is to support ventilation and oxygenation while treating the inciting cause of ARDS.


• Because ARDS is a heterogenous process of lung damage, it is important to provide lung-protective ventilation strategies to prevent vol­utrauma, barotrauma, or ventilator-induced lung injury.


• Ventilator-induced lung injuries can be prevented by reducing tidal volumes to 6 mL/kg and plateau pressure to ≤30 cm H₂O. If necessary, mild elevations in Paco₂ (permissive hypercapnia) should be accepted.


• Free radical-induced lung damage 
can be prevented by reducing oxygen delivery to ≤60% whenever possible.


PROGNOSIS


• Patients with ARDS frequently have a prolonged hospital course, which predisposes them to nosocomial infection and complications.


• Prolonged bed rest leads to significant muscle loss and functional impairment that may persist for months.


• Spirometrically evaluated lung function generally returns to normal 6 months after discharge. 


• Only 49% of patients with ARDS return to work within 1 year. JAAPA

Jami Smith is an emergency department PA and an assistant professor at Arcadia University in Glenside, Pennsylvania. Peter Sandor is a critical care PA at Saint Francis Hospital in Hartford, Connecticut, as well as an adjunct professor at Quinnipiac University in Hamden, Connecticut. The authors have indicated no relationships to disclose relating to the content of this article.