Emergency Medicine 5

Emergency Medicine 5

Part F: Dizziness and Vertigo

Basic Anatomy

• The vestibular system provides input to the brain regarding movement of the head.

The vestibular portion of the 8th cranial nerve is composed of the utricle, the saccule,

and three semicircular canals that lie at right angles to each other.

• Maintenance of equilibrium is dependent upon input from the vestibular system and

the eyes, as well as proprioception; in addition, the information must be properly

integrated in the brain. Abnormal information, or improper integration, results in a

complaint of “dizziness” or vertigo.

Scope of the Problem

• The complaint of “dizziness” can be attributed to numerous disorders, both benign and

life-threatening. The first task is to define the patient’s symptoms. Is it dizziness, vertigo

or weakness? For patients with true vertigo, the next task is to determine the source of

the symptoms; is it a peripheral or central vestibular process?

• Peripheral vestibular disorders involve structures at the level of the inner ear and the

8th cranial nerve. Central lesions involve the vestibular nuclei (located in the brainstem)

and their connections (e.g., CN III and VI nuclei, MLF).

Etiology

• Peripheral Vestibular Disorders

• Cerebellopontine angle tumor (e.g., meningioma, schwannoma)

• Acute Ramsay Hunt syndrome

• Benign paroxysmal positional vertigo (BPPV)

• Acute vestibular neuronitis/neuritis or labyrinthitis

• Perilymphatic fistula

• Post-traumatic vertigo

• Labyrinthine concussion

• Meniere’s disease

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• Central Vestibular Disorders

• Posterior fossa tumor

• Vertebrobasilar ischemia/infarction

• Multiple sclerosis

• Cerebellar hemorrhage

• Infections and parainfectious encephalomyelitis

• Wernicke’s encephalopathy

Diagnosis

History

• Ask the patient to describe the symptoms as accurately as possible: is there a spinning

sensation (i.e., true vertigo); a sense of being off balance, without spinning

(dysequilibrium); a faint feeling (near syncope); or an otherwise vague sensation of

“lightheadedness?” Patients with vestibular lesions use decriptors such as spinning, feeling

drunk or motion sick, or a sensation of imbalance (i.e., falling or tilting to one side).

Patients with nonvestibular lesions explain the feeling as one of spinning inside the head,

near-faint, floating, swimming in the head, or giddiness.

• Determine the duration of the attack—seconds, minutes, or hours to days? Peripheral

vestibular disorders are associated with intermittent episodes of vertigo that are sudden,

brief, and severe; symptoms from central lesions have a more gradual onset, last

longer, and are less intense.

• Are the episodes provoked by specific movements, position changes, or maneuvers? Peripheral

lesions are commonly initiated by turning the head to the side or tilting the

head up, whereas central causes are not positional. Symptoms of vertebrobasilar insufficiency

may be reproduced with neck movement. Valsalva’s maneuver worsens vertigo

associated with a perilymphatic fistula. Symptoms that are precipitated by stress or

certain situations (e.g., driving a car) generally indicate a nonvestibular cause. Cervical

vertigo refers to the symptom complex of neck pain, vertigo, and nystagmus that is

worse with movement of the neck.

• Are there associated symptoms? Peripheral vestibular lesions are commonly associated

with nausea or vomiting; hearing loss, tinnitus, or ear fullness; other neurologic deficits

(e.g., diplopia, dysphagia, dysarthria, extremity weakness, or sensory impairment) almost

always accompany a central lesion. Are there symptoms in the absence of vertigo?

Loss of coordination between attacks indicates 8th cranial nerve or brainstem disease.

• Has there been a recent illness? Vestibular neuritis and acute labyrinthitis are commonly

preceded by a viral illness. Is there any history of trauma? Post-traumatic positional

vertigo, labyrinthine concussion, and perilymphatic fistula are all caused by

head trauma. A rapid, twisting injury of the neck can cause vertebral artery dissection

or occlusion.

• Does the patient’s medical history suggest an etiology? Uremia, Parkinson’s disease, diabetes,

and chronic alcohol abuse are causes of peripheral neuropathy and orthostasis. Is

the patient taking any medications that may cause orthostatic hypotension (e.g., diuretics,

anti-hypertensives) or dysequilibrium (e.g., anti-convulsants, sedatives)? Is the patient

on any new medications? Frequently, elderly patients with poor vision and sensation—

especially after starting sedating medications—describe a feeling of being off balance

and stumbling (dysequilibrium), without true vertigo or presyncopal symptoms.

• Is there a history of similar episodes? What type of work-up was done, and what were

the results? Patients with ill-defined light-headedness often have extensive work-ups

without an explanation for their symptoms.

• Is there a family history (e.g., spinocerebellar degeneration, Friedrich’s ataxia,

ataxia-teloangiectasia, Wilson’s disease)?

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Physical Exam

• HEENT: Note any signs of trauma. Inspect the ears for evidence of infection, trauma, or

cerumen impaction. Are there vesicles (suggestive of VZV); is there fluid or a TM perforation?

With the patient looking straight forward, ensure that the eyes are properly aligned.

Funduscopic exam may reveal papilledema, suggesting increased intracranial pressure

from a mass lesion (usually in the posterior fossa).

• Neck: evaluate range of motion; carotid bruits suggest atherosclerosis.

• Cardiac exam: evaluate the rhythm and listen for murmurs (may suggest an outflow

obstruction).

• Neurologic Exam

• Determine the patient’s mental status.

• Abnormal cranial nerve findings suggest a central process.

• Evaluate the extraocular muscles in all six cardinal positions of gaze and look for

nystagmus. Nystagmus is described by the position of gaze in which it is provoked

and the direction of the fast component. Nystagmus associated with peripheral

disorders is generally horizontal or rotatory and does not change directions,

but is more pronounced when the patient looks in the direction of the fast

component (away from the involved side).

• Central disorders produce gaze pareses and nystagmus in any direction (including

vertical) that may change direction if the patient looks away from the direction

of the fast phase.

• Check the patient’s auditory acuity; perform Weber and Rinne tests.

• If indicated by the history, test facial nerve function. The patient with a

cerebellopontine angle tumor may have a depressed corneal reflex or facial nerve

palsy ipsilateral to the lesion.

• Lower brainstem disease may be accompanied by weakness of the tongue (CN XII),

hoarseness, dysphagia, and weakness of the palate (CN IX and X).

• Motor exam: Note any motor weakness or involuntary movements (e.g., asterixis,

myoclonus, chorea).

• Sensory exam: Proprioception and vibratory sensation are impaired in patients

with sensory ataxia produced by neurosyphilis, vitamin B12 deficiency, and polyneuropathies.

• Cerebellar exam: Tests of motor coordination evaluate cerebellar hemispheric function.

These include finger-to-nose, finger-tapping and toe tapping, rapid alternating

movements, and heel-knee-shin.

• Stance: Romberg’s sign is positive if the patient is unable to stand with the feet

together when the eyes are closed. This indicates a sensory (proprioceptive) or vestibular

disorder. Patients with vestibular lesions will fall toward the side of the lesion.

In contrast, patients with cerebellar pathology are unable to compensate with

visual cues and are unsteady with eyes open or closed.

• Gait: A wide-based, staggering gait is noted in cerebellar ataxia; in addition, tandem

gait is always impaired.

• Reflexes: hypoactive reflexes accompany cerebellar disorders and polyneuropathies

causing sensory ataxia. Multiple sclerosis, vitamin B12 deficiency, and focal brainstem

lesions are associated with hyperactive reflexes and the Babinski sign.

• Dix-Hallpike maneuver: The seated patient is rapidly lowered onto the exam table

with the head hanging off the end at a 20-degree angle. Ask the patient if he has

vertigo and examine the patient’s eyes. Slowly return the patient to a sitting position

and repeat the procedure with the head turned 45 degrees horizontally. Slowly

return the patient to sitting with the head still at a 45-degree angle; repeat the

procedure with the head turned to the other side.

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• Nystagmus associated with a peripheral vestibular disorder has a latency period

(i.e., begins several seconds after the position change); fatigues (i.e., terminates spontaneously

if the position is maintained); habituates (i.e., repeated maneuvers will

result in less pronounced symptoms); and is suppressed when the gaze is fixed. In

contrast, central vertigo is typically not positional, has no latency period, does not

fatigue or habituate, and is not suppressed by visual fixation.

Ancillary Evaluation

• Consider pulse oximetry when a systemic process is likely; in addition, patients with a

history of trauma, possible stroke, or intracranial hemorrhage (ICH) may be hypoxic.

• A bedside glucose test should be performed on all patients with neurologic symptoms.

• Serum drug levels may be useful in patients on vertigogenic medications. Consider a

toxicology screen in the appropriate clinical setting.

• Patients with dizziness or ill-defined symptoms may require further evaluation with a

complete blood count, electrolytes and other laboratories as indicated.

• Emergent noncontrast CT scan of the head is indicated in patients with a suspected

life-threatening central process (e.g., cerebellar hemorrhage, tumor, abscess, infarction).

CT may also reveal bony erosion in cases of bacterial otomastoiditis with labyrinthine

involvement.

• MRI is indicated in patients suspected of having multiple sclerosis, posterior fossa

tumor, or brainstem infarction (after negative head CT).

Differential Diagnosis

• Syncope and near-syncope

• Hypovolemia from any cause

• Acute coronary syndrome

• Intoxication

• Hyperventilation syndrome

• Anxiety and affective disorder

• Dysequalibrium

• Metabolic disorders

• Sepsis

• Intracranial pressure

Treatment

• Peripheral Vestibular Disorders

• Vestibular suppressants are useful in the acute period. Prolonged use may impede

central compensation. Therefore, only a three-day supply should be prescribed

(Table 4F.1).

• Vestibular exercises facilitate the central compensation process and may be useful

for patients with chronic vertigo or recurring BPPV. The patient should assume a

position with his head that causes nystagmus, and then attempt to focus the eyes

and move them in a position that maximizes his symptoms. As the nystagmus diminishes,

the patient should begin to move the head up and down or from side to

side while visually fixating on a target. He should attempt to stand and walk while

the nystagmus is still present, and (as symptoms improve) should move the head

from side to side or up and down while walking (first slowly, then quickly in all

directions). Compensation may take several months.

• Specific treatment

• The Canalith repositioning maneuver is effective in cases of BPPV resulting

from otoconia. Details of this procedure are described elsewhere. Note that patients

may have an increase of symptoms as a result of repositioning maneuvers.

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Furthermore, feasibility of patient education in a busy ED may be an issue.

Otolaryngology follow-up is advised.

• Acute peripheral vestibulopathy encompasses vestibular neuritis and acute labyrinthitis

of unknown etiology (but commonly preceded by a viral infection).

Both disorders are associated with acute onset vertigo and nystagmus, nausea,

and vomiting that may last for 2 wk. The distinction between the two is based on

the presence (labyrinthitis) or absence (neuritis) of concomitant hearing loss or

tinntus. A 3-day course of a vestibulosuppressant with bed rest is recommended.

In addition, a 10-day course of prednisone may shorten the course of the illness.

• Ramsay Hunt syndrome is a reactivation of varicella-zoster that can involve multiple

cranial nerves (including V, VII, VIII, IX and X). Prednisone and acyclovir

have been found to facilitate recovery, if treatment is initiated within 3 days (compared

to more than 7 days) after symptom onset.

• Prednisone 60 mg PO q day, tapered over 10 days

• Acyclovir 400 mg PO 5x/day for 10 days

• Meniere’s disease is thought to be caused by excessive fluid within the inner ear.

It is characterized by acute attacks of vertigo and ear pressure lasting hours, associated

with tinnitus and sensorineural hearing loss. In addition to

vestibulosuppressants, patients may benefit from restricted sodium, caffeine, and

nicotine intake. All patients with Meniere’s disease should be referred to ENT.

• The patient with dysequilibrium caused by multiple sensory deficits functions

better with improved lighting, elimination of sedating medications, and (in the

short term) using a walker. He may benefit from a referral for vision refraction or

rehabilitation, as indicated by his deficits.

Disposition

• Patients with neurologic deficits or suspected central disorders should be admitted. Patients

with intractable vomiting or severe dehydration may require inpatient treatment.

• Patients with suspected peripheral vestibular disorders who are discharged home with

medication should be instructed to follow-up with their PCP if symptoms persist

more than a few days.

Suggested Reading

1. Baloh RW. Dizziness: Neurological emergencies. Neurol Clin North Am 1998; 16:2.

2. Disorders of equilibrium. In: Simon RP, Aminoff MJ, Greenberg DA, eds. Clinical Neurology

4th ed. Stamford: Appleton and Lange, 1999.

3. Herr RD. Dizziness and vertigo. In: Howell JM, ed. Emergency Medicine. Philadelphia:

WB Saunders Company, 1998.

4. Tusa RJ. Vertigo. Neurol Clin 2001; 19:1.

Table 4F.1. Treatment options in peripheral vertigo

Antihistamines Meclizine 25 mg PO q6h

Diphenhydramine 25-50 mg PO q6h

Phenothiazines Prochlorperazine 5-10 mg PO q6-8h; 25 mg PR q12h

Promethazine 25-50 mg PO/IM q4-6h;

Anticholinergics Scopolamine 0.5 mg transdermally q 3 days

0.4-0.8 mg PO q6-8h

Benzodiazepines Diazepam 5-10 mg PO q6-8h

Serotonin antagonists Ondansetron 4 mg PO q 8 h

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Part G: Seizures

Etiology/Risk Factors

• Head Trauma

• Depressed skull fracture

• Subdural hematoma, intracerebral hemorrhage

• Infectious

• Meningitis, encephalitis, abscess

• Vascular

• Stroke or vascular malformations

• Hypertensive encephalopathy

• Eclampsia

• Environmental

• Hyperthermia

• Toxic

• Drug overdose or withdrawal

• Neoplasm

• Metabolic

• Hypoglycemia

• Hypo- or hypernatremia

• Hypo- or hypercalcemia

• Uremia; hepatic encephalopathy

• Hyperosmolar states

• Congenital

• Idiopathic epilepsy

• Hematologic

• Porphyria

• Neurologic

• Febrile seizures

• HIV encephalopathy

• Global cerebral ischemia

Scope of the Problem

• Nearly 1% of all emergency department visits are due to new-onset generalized seizures

in adults. Seizure may be the sole presenting symptom of a life-threatening illness

requiring immediate treatment.

• Seizures are defined as disordered discharges of cerebral neurons. The outward expression

of a seizure may take many forms:

• Generalized seizures involve a loss of consciousness.

• Tonic-clonic seizures are characterized by a phase of tonic muscle contractions causing

extension of the limbs (and falling) and cessation of ventilatory effort, followed by

a clonic phase of rhythmic muscle contraction and relaxation resulting in symmetric

jerking of the limbs with return of spontaneous respirations. Urinary incontinence

may occur. A postictal phase of unconsciousness or confusion is not uncommon.

It usually clears within 30 min, but may last for hours.

• Absence seizures are characterized by a brief (5-10 second) loss of consciousness,

during which postural tone is maintained. Blinking or head turning may be the

only motor manifestation of the seizure. There is no postictal period of confusion.

• Partial Seizures

• Simple partial seizures begin within a specific region of the cortex, which determines

the symptoms (i.e., sensory, motor, or autonomic). The symptoms may

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sponteously resolve, recur, spread to contiguous cortical regions (jacksonian march),

or become secondarily generalized. In the absence of generalization, there is no loss

of consciousness.

• Complex partial seizures cause impaired consciousness. Patients experience the same

symptoms during each successive ictal event. The episode classically begins with a

blank stare, and (occasionally) loss of muscle tone, resulting in a fall. Epigastric

sensations are most common, but affective, cognitive, or sensory symptoms also

occur. Automatisms are common and can be simple (e.g., chewing, blinking, laughing)

or complex (e.g., vocalizations or repetitive movments). Secondary generalization

may occur so rapidly that the preceding partial component is not recognized,

and only the altered mental status is observed. A postictal period is common but

usually short (i.e., minutes).

Diagnosis

History

• If the seizure activity has terminated prior to the patient’s arrival in the emergency

department, a description of the event from a reliable witness is invaluable. Any history

of trauma (recent or remote) should be elicited. A description of events immediately

preceding the seizure activity should also be sought, including any complaints of

pain or focal neurologic deficits. Attempt to determine whether the patient was injured

during the episode (e.g., fall).

• Obtain the patient’s medical history, if possible, including a prior history of seizures or

other medical conditions, medications, or recent symptoms (e.g., infections). Ask about

the use of drugs or alcohol, or exposure to other toxins.

Physical Examination

• Include a rectal temperature with the vital signs.

• Look for evidence of trauma, either as a cause or a result of the seizure. A detailed neurologic

examination should be performed. If the patient has an altered level of consciousness,

is he in a postictal state? Or is there another cause? Are there any focal neurologic

deficits? Look for signs of increased intracranial pressure (ICP) (e.g., papilledema). Is

there evidence of a CNS or systemic infection? Are there other signs of systemic illness?

Is there evidence of a toxic exposure? Serial neurologic exams are critical.

Differential Diagnosis

Toxic and metabolic Hypoglycemia; renal or hepatic dysfunction

encephalopathies with Recreational drug use; alcoholic blackouts

fluctuating consciousness Delerium tremens

Syncope Neurocardiogenic; vasovagal; orthostatic; cardiac

Cerebrovascular TIA (incl. vertebrobasilar insufficiency)

Movement disorders Dystonias

Tonic spasms with tetanus, strychnine, and camphor

Tic disorders; tremor

Benign nocturnal myoclonus

Asterixis with hepatic and renal failure

Rabies

Transient global amnesia

Migraine (including acephalgic migraine)

Paroxysmal endocrine Pheochromocytoma; carcinoid syndrome

disturbances

Sensory disturbances Visual hallucinations with visual field loss

Paroxysmal vertigo

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Sleep disorders Apnea

Night terrors; sleep walking

Narcolepsy; hypersomnia

Psychogenic Hyperventilation; breath-holding spells in children

Panic attacks; episodic dyscontrol; dissociative states

Conversion disorder; hysteria; malingering; psychosis

Obsessive-compulsive disorder

Pseudoseizure

Evaluation

As with the work-up of any presenting sign(s) or symptom(s), the use of diagnostic

tests should be guided by the history and physical examination of each patient

who presents with seizure activity. When a differential diagnosis is formulated for a

particular patient, the following studies may be helpful in ruling in or excluding

specific etiologies:

• Laboratory

• Glucose should be checked on all first-time seizure patients. Although commonly

ordered, routine electrolytes, calcium and magnesium have low diagnostic yield in

otherwise healthy patients with a first seizure. Consider these studies when clinically

indicated.

• A pregnancy test is indicated in all females of reproductive age.

• Antiepileptic drug (AED) levels

• A more extensive work-up is appropriate in patients with a history of alcohol abuse,

to include CBC, PT, electrolytes, BUN, and creatinine. A blood alcohol level and

toxicology screen should also be considered.

• Magnesium levels should also be checked in patients with diabetic ketoacidosis.

• Coagulation studies are recommended in patients on anticoagulants, with a known

coagulopathy, or with a history of platelet disorders.

• Lumbar puncture is indicated in the following situations:

• Persistent alteration in mental status or status epilepticus (after patient is stabilized).

• Signs of CNS infection (nuchal rigidity, petechiae)

• Severe headache (i.e., when unruptured aneurysm or SAH is suspected)

• In a patient with a history of cancer and negative CT scans (leptomeningeal

metastases?)

• History of immunosuppression, without an identifiable cause for the seizure

(i.e., lab or radiographic abnormality)

• Children with recent antibiotic use

• Adults with fever, without an infectious source (neutropenic patients excluded)

• Imaging

• Emergent noncontrast CT scan of the head is indicated in all first-time seizure

patients without an identifiable, nonstructural cause (e.g., hypoglycemia, febrile

seizure). The following factors increase the likelihood of an abnormal CT:

• A focally abnormal exam or signs of increased ICP

• Multiple or focal seizures

• Higher likelihood of structural abnormalities (i.e., increased age, history of head

trauma, HIV/other immunocompromised states, cancer, alcohol abuse, anticoagulation,

vascular disease, demographic risk of cysticercosis)

• Previous CNS disorders

• Subtherapeutic antiepileptic drug levels are the most common cause of recurrent

seizures. Indications for CT scan in patients with a previously diagnosed seizure

disorder include:

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• Change in seizure pattern without a known cause

• Persistently altered mental status or prolonged postictal confusion

• New focal neurologic deficits

• Contrast-enhanced head CT should be performed in immunocompromised patients

and those with a history of malignancy (after a negative noncontrast CT).

• MRI is recommended, on an elective basis, if the screening CT is negative.

• EEG

• EEG is generally not readily available in the ED and usually is not required in the ED

work-up of seizures. However, in the following cases, emergent EEG is indicated:

• The seizure appears to have terminated, but the patient remains altered.

• Status epilepticus is suspected (convulsive or nonconvulsive).

• EKG

• Seizure may be the presenting symptom of hypoxia in a patient with a dysrhythmia

resulting from myocardial ischemia. EKG should be considered in patients with

known or suspected coronary artery disease.

• Patients with long QT syndrome frequently present after a syncopal or ictal event.

Congenital long QT syndrome is seen in children or young adults who may have a

family history of syncope or early cardiac death, or a personal history of congenital

deafness. Long QT syndrome may be acquired and is a side effect of tricyclic antidepressants,

phenothiazines, and amiodarone. Associated EKG abnormalities include

prolonged or abnormal T waves and bradycardia.

Treatment

• As with any patient in the ED, attention to the patient’s airway, breathing, and circulation

is paramount. The patient should be positioned in such a way as to protect the

airway in case of vomiting, and suction should be readily available. Supplemental

oxygen should be administered by nasal cannula or face mask, and the patient placed

on continuous pulse oximetry.

• If trauma is a concern, the cervical spine should be immobilized.

• As soon as possible, intravenous or intraosseous access should be obtained so that fluids

and medications can be given. The patient should be placed on a cardiac monitor.

• Underlying, correctable etiologies should be rapidly identified and treated.

• Benzodiazepines are the agents of choice to acutely terminate seizure activity,

although the necessity of this practice as routine is debatable. Most seizures are

brief (<2 min) and there is no evidence that a single, brief seizure has deleterious

central nervous system effects. Several agents are available (see Table 4G.1).

• Diazepam is highly lipophilic and thus crosses the blood-brain barrier rapidly. It is

usually administered via the intravenous route but is equally effective when given

rectally. Other routes include oral and endotracheal. The median time to terminate

seizure activity after injection is 2 min. However, its antiepileptic activity lasts only

20 to 30 min. Depending upon the clinical setting, a longer acting AED may be

necessary after administration of diazepam.

• Lorazepam is less lipid soluble than diazepam but has a similar time to seizure

control (3 min). Its antiepileptic activity lasts 12-24 h, negating the need to administer

an additional AED if seizure activity is terminated. Acceptable routes of administration

include intravenous, rectal, sublingual, and oral.

• Midazolam is used less frequently but is another option. Unlike diazepam and

lorazepam, this agent is well absorbed when given via the intramuscular route because

of its water-solubility. After administration, it becomes lipid soluble and, like

diazepam, has rapid penetration of the blood-brain barrier as well as a short duration

of antiepileptic activity. Acceptable routes of administration include intranasal,

intramuscular, intravenous, rectal, and buccal.

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• Initiation of a long-term AED for a first seizure should be considered in certain settings.

Close neurologic follow-up is indicated for these patients. All AEDs have adverse side

effects and “label” the patient. If there is any question as to the necessity of initiating

chronic therapy, neurologic consultation is advised. Multiple AEDs are available—a comprehensive

discussion is beyond the scope of this writing. Consider initiation of an

AED in the following cases:

• An underlying cause that can’t be promptly treated (e.g., tumor)

• A patient at risk for recurrent seizures (e.g., cysticercosis, penetrating head injury)

• Presence of an identifiable, remote cause (debatable)

• Patients with a history of recent (<2 yr) seizure that went untreated

Status Epilepticus (SE)

• SE has classically been defined as persistent seizure activity for 30 min or recurrent

seizures without full recovery between events. Since most isolated ictal events last <2

min, a more practical definition for SE is seizure activity that persists for 5 min or more.

• SE is not a disease in itself, but rather a manifestation of another illness. One of the

goals when treating SE is to identify and address acute precipitants. In adults, the most

common cause of SE is noncompliance with AEDs. In children, congenital abnormality

and infection are the most common.

• The earlier that treatment for SE is initiated, the easier it is to control. In addition, the

following complications may be avoided.

• Autonomic dysfunction including hypertension, tachycardia, and hyperthermia

• Vertebral and other fractures; shoulder dislocations

• Rhabdomyolysis

• Aspiration pneumonia

Table 4G.1. Antiepileptic agents for status epilepticus

Medication Dose (IV) Side Effects

Midazolam 0.2 mg/kg then Respiratory depression, hypotension,

0.05-1.0 mg/kg/h sedation

Tachyphylaxis with prolonged

infusions

Diazepam 0.2 mg/kg (up to 20 mg in Respiratory depression, hypotension,

adults) sedation

Lorazepam 0.1 mg/kg (usual maximum Respiratory depression,

dose 8 mg) hypotension, sedation

Phenytoin 20 mg/kg @ 50 mg/min Hypotension, atrioventricular

May give additional 5-10 block, dysrrhythmias

mg/kg Soft tissue necrosis, sterile

abscess with IM use or

extravasation

Fosphenytoin 20 mg/kg PE* @ 150 mg/min Hypotension and pruritis

May use same dose IM

Phenobarbital 20 mg/kg not to exceed 100 Respiratory depression, apnea,

mg/min hypotension

Propofol 1-3 mg/kg then 2-10 Respiratory depression,

mg/kg/h hypotension

Pentobarbital 3-5 mg/kg then 1-5 mg/kg/h Respiratory depression, apnea,

hypotension, myocardial depression,

weakness during recovery period

* Phenytoin equivalent

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• Metabolic derangements

• Cerebral edema

• Treatment (see Table 4G.1)

• All patients require appropriate supportive care. If intubation is required, short-acting

paralytics are preferred in order to allow the practitioner to identify ongoing seizure

activity.

• Benzodiazepines are first-line therapy for SE. Because of its duration of action, lorazepam

is preferred. Adequate dosing is imperative. If SE is not controlled with an appropriate

dose of benzodiazepine, it is unlikely that subsequent doses or use of another benzodiazepine

will be effective.

• Phenytoin is a long-acting AED that is effective for both SE and chronic maintenance

therapy. Phenytoin is generally the preferred second-line agent for SE if benzodiazepines

have failed. Side effects of the intravenous preparation are attributed to the propylene

glycol diluent. These are minimized by infusing at a rate not to exceed 1 mg/kg/

min in children and 50 mg/min in adults. Fosphenytoin is a phosphorylated ester of

phenytoin. It is highly water-soluble, and is rapidly converted to phenytoin after administration.

It is rapidly and completely absorbed when given intramuscularly and can

also be given intravenously at three times the rate of phenytoin. Because it has no intrinsic

action before conversion, it is believed to have the same onset of action as phenytoin.

Its primary disadvantage is cost, averaging twenty-fold more than phenytoin.

• Phenobarbital, a long-acting barbiturate, may lead to hypotension as well as profound

respiratory depression and apnea. Rate of infusion should not exceed 100 mg/min. It

is generally reserved for cases in which benzodiazepines and phenytoin have failed.

• Agents for refractory SE—All patients with refractory ictus require EEG monitoring as

well as ventilatory support. Pressors may also be necessary in the setting of hypotension.

• Midazolam—Discussed above

• Propofol—This is a nonbarbiturate anesthetic agent that also has antiepileptic effects.

It has a rapid onset of action and a quick recovery time after the drug is

discontinued.

• Pentobarbital—This barbiturate has more pronounced side effects than both

midazolam and propofol. Patients will often require pressors because of significant

hypotension and myocardial suppression.

• Adjunctive therapy—Includes both pyridoxine and magnesium.

Disposition

• All patients with SE require ICU admission.

• Patients with neurologic disorders, systemic disease or electrolyte abnormalities (e.g.,

neurosurgical lesions, CNS infection, hepatic or renal dysfunction, hyponatremia)

require admission and management of the underlying disease process.

Suggested Reading

1. Bradford JC, Kyriakedes CG. Evaluation of the patient with seizures: An evidence based

approach. Emerg Med Clin North Am 1999; 17:1.

2. Haafiz A, Kissoon N. Status epilepticus: Current concepts. Ped Emerg Care 1999; 15:2.

3. Hanhan UA, Fiallos MR, Orlowski JP. Status epilepticus. Ped Clin North Am. 2001; 48:3.

4. Krohmer JR, Sheets CA. Seizures. In: Hamilton GC, ed. Presenting Signs and Symptoms

in the Emergency Department. Evaluation and Treatment. Baltimore: Williams

and Wilkins, 1993.

5. Roth HL, Drislane FW. Seizures. Neurol Clin North Am 1998; 16:2.

6. Seizures and syncope. In: Simon RP, Aminoff MJ, Greenberg DA, eds. Clinical Neurology

4th ed. Stamford: Appleton and Lange, 1999.

7. Yoon Y, Jagoda A. New antiepileptic drugs and preparations. Emerg Med Clin North

Am 2000; 18:4.

CHAPTER 1

CHAPTER 5

Emergency Medicine, edited by Sean Henderson. ©2006 Landes Bioscience.

GI Emergencies

Susan Stone and Andrew S. Kassinove

Introduction

Abdominal pain accounts for over five million visits annually to Emergency Departments.

Between 20-40% of these patients will require inpatient admission. However,

it is often difficult to arrive at the etiology of abdominal pain in the course of

the ED visit. In particular, women who are of child-bearing age or pregnant, children

and elderly patients create a diagnostic challenge (due to atypical presentations).

Unfortunately, many of the disease processes share similar clinical presentations

and may be difficult to sort out by history alone. Physical examination and laboratory

evaluation can both lack sensitivity, making the job of the emergency physician

difficult. Therefore, the diagnosis of abdomen pain of unclear etiology is a common

diagnosis made in cases where the underlying pathology is not clear. This obligates

the physician to provide patients with adequate reexamination to monitor the progression

of the process.

While the discussion of abdominal disorders in this chapter is not exhaustive, the

most common etiologies are reveiwed.

As a general rule, elderly patients presenting with abdominal pain form a unique

group. Despite lack of identification of a focal disease process on initial presentation,

at least half will have a disorder requiring surgical intervention. Physical examination

will often lack sensitivity, as will laboratory evaluation. Women of

child-bearing age and young children will have atypical presentations of common

disorders, such as appendicitis and may require more observation time.

Despite technology in imaging and laboratory diagnostics, a large portion of patients

will still have undifferentiated abdominal pain, requiring close follow-up and

referral.

Mesenteric Ischemia

Risk Factors/Etiology

• Age >50 yr old

• Occlusive disease (80% of mesenteric ischemia) occurs 50% of the time from the

sudden occlusion of the superior mesenteric artery originating from a proximal source

and 25% of the time as local thrombosis. Mesenteric venous thrombosis is the cause

only 5% of the time. Prolonged occlusion can result in both proximal and distal

reactive vasospasm, further aggravating the insult to the intestines.

• Occlusive disease often results from the propagation of left atrial or ventricular thrombi

that fragment during or after a dysrhythmia or from atherosclerotic disease at the

origin of the SMA itself. Thus, the major risk factors are recent MI, peripheral vascular

disease, and cardiac dysrhythmias. Mesenteric venous thrombosis occurs during

the classic hypercoagulable states as well as during malignancy, abdominal trauma,

and estrogen therapy.

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• Nonocclusive disease (20% of mesenteric ischemia) occurs during low flow states, such

as cardiogenic shock, hypovolemia, or sepsis resulting in reactive vasoconstriction of

the splanchnic circulation. Additionally, regional vasospasm can result from use of

vasoactive medications, such as digoxin, diuretics, cocaine, or vasopressin.

Clinical Presentation and Diagnosis

• The historical factors may be nonspecific, but the diagnosis should be pursued in any

person >50 yr old with sudden onset of acute abdominal pain and with an associated

low flow, atherosclerotic, or hypercoaguable disease state.

• Historical factors include abdominal angina, recent weight loss, or recent change in

bowel habits.

• Signs and symptoms include nausea and vomiting, colicky, severe, diffuse abdominal

pain associated with repeated bowel movements, and a diffusely tender abdomen. As

the disease progresses peritoneal signs occur and are an ominous finding. Abdominal

distention and rectal bleeding may be the only initial complaint in up to 25% of the

cases. The only initial abnormality on physical exam may be the presence of fecal

occult blood, occurring in over half of the cases.

• Laboratory tests are nonspecific. An elevated WBC count is common, but a normal

count does not exclude the diagnosis. Additionally, metabolic acidosis with a base

deficit, an elevated amylase, and evidence of hemoconcentration are sensitive (present

in more than half the cases) but nonspecific findings.

• Plain radiographs are often normal early on but may be used to rule out other pathology.

They may show pneumatosis intestinalis, portal vein gas, or thumb printing in

late disease. CT scan and ultrasound may show edema of the bowel wall and mesentery,

ascites, abnormal gas patterns, and evidence of mesenteric venous thrombosis.

CT is 82% sensitive and 93% specific and is better than angiography for venous obstruction.

Ultrasound is only 28% sensitive.

• Angiography remains the diagnostic gold standard with a sensitivity of 88% (92%

arterial and 50% venous). Angiography is contraindicated in shock states or with

patients on vasopressor therapy because they confound the diagnosis of nonocclusive

mesenteric ischemia. False negative studies are common with mesenteric venous

thrombosis.

• The differential diagnosis is large and includes all sources of acute abdominal pain,

especially ruptured abdominal aortic aneurysm, perforated dudodenal ulcer, strangulated

bowel obstruction, and urolithiasis. Common initial misdiagnoses include constipation,

gastroenteritis, ileus, and small bowel obstruction.

Treatment

• Stabilization of the patient is of the utmost priority, with initial focus on the ABCs.

Hypovolemia is common and should be corrected. Vasoactive drugs should be discontinued.

CHF and dysrhythmias should be managed. A nasogastric tube should be

placed for early decompression. Broad spectrum antibiotics should be begun early.

• Surgical consultation should be obtained immediately.

Abdominal Aortic Aneurysm (AAA)

Risk Factors/Etiology

• The diagnosis of aortic aneurysms has increased, reflecting an aging population and

more liberal use of CT scan and ultrasound. However this diagnosis is frequently

overlooked.

• It is necessary to classify the aneurysm as intact, ruptured or contained rupture.

• This process occurs most frequently in elderly patients over 65 yr of age.

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• Risk stratification shows that males, tobacco use, atherosclerosis and hypertension are

important predisposing factors. By age 80, 6% of men will have AAA. Younger patients

with collagen vascular disease are also at risk of aortic dissection.

• Blunt abdominal trauma less commonly results in an aortic aneurysm.

• Patients with preexisting aortic grafts and those with immunosuppression may develop

mycotic infections, where the aorta becomes infected and may rupture.

• Aneurysms result from dilatation of the aortic wall with an increase in diameter by

over 50%. This dilatation is a mechanism of the artery to compensate for a proximal

stenosis. Once the aneurysm exceeds 5 cm, the risk of rupture is up to 40%. The 5 yr

survival after repair is almost 70%.

Clinical Presentation

• Classical presentation of pulsatile mass in the patient with abdominal pain and pulse

deficits is not always present.

• Syncopal episodes with hypotension or transient hypotension alone in the elderly patient

with abdominal pain should raise suspicion.

• Hematuria may result from dissection of the renal arteries. Over 95% of AAA will be

infrarenal.

• Pulse deficits

•. Patients presenting with an abdominal aneurysm with abdominal pain are ruptured

until proven otherwise and surgical consult is mandatory. Use caution with results of

CT scanning, as this may miss a rupture or leak of the aneurysm.

If an aneurysm is identified on ultrasound or CT scan, the patient needs to be followed

by a vascular surgeon.

Treatment

Management is broken down into three categories:

1. Asymptomatic: serial ultrasounds and close follow-up

2. Rupture stable: CT scan and surgical repair

3. Rupture unstable: surgical repair

The differentiation between a stable and unstable rupture is trivial as the process

is dynamic. Therefore early surgical consultation is critical.

The perioperative mortality is over 25% secondary acute myocardial infarction in

emergent surgery compared to fewer than 5% for elective. Therefore it is preferred,

but not always possible, to prime the patient for the operating room.

Bowel Obstruction

Risk Factors/Etiology

• Small bowel obstruction is typically caused by postoperative adhesions, hernias, or

tumors.

• Large bowel obstruction is caused by carcinoma, diverticulitis, volvulus, inflammatory

bowel disease, radiation colitis, or foreign bodies. It is primarily a disease of the elderly.

• Sigmoid volvulus in the United States occurs in debilitated elderly people secondary

to chronic severe constipation.

• Cecal volvulus is most common in 25-35 yr olds but may occur at any age. It is likely

due to a hereditary hypofixation of the cecum to the posterior abdominal wall. Risk

factors include marathon running, pregnancy, and prior abdominal surgery.

Clinical Presentation and Diagnoses

• Acute onset of severe intermittent abdominal pain followed by nausea and vomiting is

the common clinical manifestation. Vomiting may be absent in distal obstructions.

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The abdomen is diffusely tender and becomes progressively distended. Obstipation

may be absent early on or in a partial obstruction, and its absence does not exclude the

diagnosis. Peritoneal signs or fever suggest strangulation or perforation.

• Signs include a tympanitic distended abdomen, high pitched “tinkling” bowel sounds,

or a tender mass in closed loop obstructions.

• Laboratory values are nonspecific. An elevated WBC count may be present in both

simple and strangulated obstructions. Electrolyte abnormalities are late findings. Hemoconcentration

may reflect third spacing of fluid.

• Plain radiographs are often diagnostic, demonstrating small bowel obstruction (SBO)

in 50-60% of cases and suggesting it in 20-30% more. A supine abdominal film along

with either a lateral decubitus or upright abdominal films are minimally needed for

diagnosis. An upright chest film may be added to search for free air under the diaphragm

indicating a perforated viscous. CT scan is 94% sensitive and 83% specific in

diagnosing SBO. Ultrasound is 88% sensitive and 96% specific in diagnosing SBO.

Plain abdominal films are the test of first choice.

• In small bowel obstruction, distension of the small bowel is seen, often with distal

collapse. The small bowel is differentiated from the large bowel by the presence of

“valvulae conniventes” which are numerous, narrowly spaced and cross the entire lumen.

A “string of pearls” sign is highly suggestive of small bowel obstruction and is

described as a line of air pockets in a fluid filled small bowel. Air fluid levels in a

stepladder pattern are also suggestive of a small bowel obstruction.

• A large bowel obstruction is suggested by dilation of bowel with “haustra”, which are

widely spaced, do not cross the entire lumen, and are less numerous than the “valvulae

conniventes.” A sigmoid volvulus is diagnosed by a single dilated loop of large bowel

in the mid abdomen in the classic “bent inner tube” configuration, 80% of the time.

If not, sigmoid volvulus can be diagnosed by the classic “birds beak” sign on barium

enema. Distended large bowel in the left lower quadrant with absence of right-sided

gas may indicate a cecal volvulus.

• Differential diagnoses include gastroenteritis, mesenteric ischemia, adynamic ileus,

and incarcerated hernia. The intermittent nature of the pain is suggestive of bowel

obstruction but is also present in mesenteric ischemia.

Treatment

• Early nasogastric decompression, aggressive fluid resuscitation, broad spectrum antibiotics

including coverage of Gram negatives and anaerobes, and early surgical consultation

are the mainstays of treatment of small and large bowel obstructions. Up to

75% of partial small bowel obstructions and up to one-third of complete small bowel

obstructions will resolve with decompression and fluid resuscitation alone. Strangulated

obstructions indicated by fever, tachycardia, and/or localized tenderness are operative

cases. Uncomplicated obstructions are usually initially treated conservatively,

with surgery reserved for treatment failures.

• Octreotide may be useful in nonoperative cases of bowel obstruction by decreasing GI

secretions and motility.

• Sigmoid volvulus is treated with rectal tube decompression or surgery and usually

does not require aggressive fluid resuscitation as there is little third spacing. Cecal

volvulus often requires surgery.

Disposition

• These patients are all admitted to the hospital, almost always under the care of a surgeon.

• “Never let the sun rise or set on a bowel obstruction.”

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Acute Appendicitis

Risk Factors/Etiology

• Appendicitis has a yearly incidence of 1/1000 persons with a lifetime incidence of 7%.

There is a slightly increased incidence in males. The highest incidence occurs in 10-30

yr olds, with atypical presentations more common in the very young or very old and

women of child-bearing age.

• Appendicitis is the most common surgical emergency in children.

Clinical Presentation and Diagnoses

• The classic description is of periumbilical, epigastric, or diffuse dull pain migrating

over several hours to McBurney’s point in the right lower quadrant, with the pain

changing in character from dull to sharp as the overlying peritoneum becomes inflamed.

Peritoneal signs, including involuntary guarding, rigidity and diffuse percussion

tenderness may indicate perforation.

• The pain is less likely to be appendicitis if it has been ongoing for more than 72 h.

• Associated symptoms which increase the likelihood of appendicitis are anorexia or

nausea and vomiting following the onset of abdominal pain. Less specific and less

frequently associated symptoms include fever, chills, diarrhea, dysuria and frequency,

and constipation. Constipation is a more common symptom in the elderly.

• The location of the pain is highly variable. 20% of surgically proven appendicitis

presents without right lower quadrant pain. Retrocecal appendices or those displaced

in pregnancy may cause flank pain. A pelvic appendix may irritate the bladder, resulting

in suprapubic pain or dysuria, while a retroileal appendix may irritate the ureter,

causing testicular pain. More than two-thirds of appendices lie within 5 cm of

McBurney’s point, with more inferior and medial.

• Frequently associated signs include low-grade temperature, abdominal, rebound, rectal,

or cervical motion tenderness. Less commonly present are the psoas and obturator

signs or a palpable mass.

• Associated laboratory values include a WBC count >10,000 and less frequently pyuria

(>5 WBC’s/hpf). However, between 10-60% of patients will initially have a normal

white count.

• C-reactive protein (CRP) has been shown to be elevated in several studies when used

serially to be helpful in excluding appendicitis, with the diagnoses being rare with two

normal values drawn 12 h apart. However, one isolated value is neither sensitive nor

specific.

• Perforation rates are commonly quoted at 20%, with children and elderly incurring perforation

>70% of the time. Perforation is the most common malpractice claim for abdominal

emergencies and the fifth most expensive claim overall in emergency medicine.

• Diagnostic studies are merely ancillary and should not replace the clinical impression.

Abdominal plain films have little or no utility and should not be routinely ordered, as

even the finding of an appendicolith are neither sensitive nor specific for appendicitis.

An upright CXR finding of free air is neither sensitive nor specific for perforated

appendicitis.

• The two radiologic studies to consider in cases of diagnostic uncertainty are abdominal

ultrasound and helical CT. Ultrasound has reported sensitivity up to 93% and specificity

up to 95% and is the preferred test in children and pregnant women. Triple contrast

oral, rectal, and IV CT of the abdomen has a sensitivity approaching 100% and specificity

of 95-98% when used with the latest CT scanners and experienced readers.

Noncontrast helical CT has a sensitivity of 90% and a specificity of 91%.

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• Additionally, some institutions are using the laparoscope to quickly look inside

the abdomen. However, this technique often leads to open laparotomy. Less widely

available, Technetium-99m labeled WBC scans have a reported sensitivity of 98%

and specificity of 95% but are time consuming.

• Serial abdominal exams over 6-12 h will often aid in the diagnoses as the pain of

appendicitis is progressive, leading to the diffusely tender, often rigid abdomen of a

perforation. Several studies have shown observation is safe and effective.

• A urine pregnancy test should always be obtained in all women of child-bearing age.

• Uncommon mimics of acute appendicitis include DKA and Streptococcal pharyngitis

in young children. Other diagnoses to consider include testicular torsion, ruptured

ectopic pregnancy, peptic ulcer disease, billiary tract disease, diverticulitis, abscesses,

renal colic, pyelonephritis, bowel obstruction, and abdominal aortic aneurysm.

Treatment and Disposition

• High clinical suspicion: IV fluids if dehydrated, NPO, antibiotics (Cefotetan or

Cefoxitan), early surgical consultation with early appendectomy.

• Moderate clinical suspicion: IV fluids if dehydrated, NPO, surgical consultation, adjunctive

test (ultrasound or CT scan). If CT scan or ultrasound positive then early appendectomy

and antibiotics. If negative, then observation with serial abdominal exams.

• Low clinical suspicion: surgical consultation, follow-up in 12 h or earlier if symptoms

persist or worsen.

• Acceptable negative appendectomy rates are approximately 20%.

Colonic Diverticulitis

Risk Factors/Etiology

• 96% of patients are older than 40 yr of age.

• Most commonly confined to the sigmoid colon.

• Almost exclusively found in western civilizations, due to a relatively low fiber diet.

• 50% of people older than 65 will have diverticula, with 10-20% of those eventually

developing diverticulitis.

• Inflammation occurs when fecal matter is trapped in a diverticular sac.

Microperforations in the colon then occur producing a pericolic abscess or even

peritonitis.

Clinical Presentation and Diagnoses

• Persistent abdominal pain, initially vague and diffuse, later localizing to the left lower

quadrant is the most common presentation of sigmoid diverticulitis.

• Constipation, low grade fever, and malaise are common. Dysuria and frequency are

also common due to irritation of the nearby bladder and ureter. Less common are

nausea, vomiting, anorexia, or diarrhea.

• Exam will reveal left lower quadrant tenderness and may reveal peritoneal signs if

significant spillage of bowel contents has occurred. A mass may occasionally be palpated.

The rectal exam may reveal local tenderness and will often be fecal occult blood

positive.

• An elevated WBC count with a left shift is common. Iron deficiency anemia is uncommon

and should prompt a look for other causes, such as carcinoma.

• The diagnoses of sigmoid diverticulitis are often made on clinical grounds alone.

Other diagnostic modalities include plain abdominal films to rule out obstruction,

followed by CT with oral contrast, IV, and rectal contrast, to confirm the diagnoses

(sensitivity and specificity approaching 100%), look for an abscess, and rule out

other pathology such as appendicitis or carcinoma. An upright chest X-ray may also

be obtained to look for free air under the diaphragm, signaling a perforated viscus.

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Graded compression ultrasound has a sensitivity of 84-98% and a specificity of

93-97% for diverticulitis. Barium enema is not recommended as it may increase the

chance of perforation.

• Cecal or right-sided diverticulitis is difficult to distinguish from appendicitis. Other

diagnoses high in the differential include colon carcinoma with localized perforation,

ischemic colitis, ulcerative colitis, and bacterial colitis.

• Complications include abscess or fistula formation, perforation, or colonic obstruction.

Colovesicular fistulas present with pneumaturia, fecaluria, dysuria, frequency, or

incontinence. Colonic obstruction is rarely complete.

Treatment

• Most episodes can be managed medically with admission to the hospital for bowel

rest, IV antibiotics and fluids and analgesics.

• Antibiotic regimens must cover both anaerobic and Gram-negative bacteria. Regimens

may include Cefoxitin 2-3 g IV q 8 h or triple therapy with Ampicillin,

Gentamycin, and Metronidazole.

• Mild disease in reliable patients may be treated as an outpatient with cephalosporins

or quinilones, pain medicine, a clear liquid diet and early follow-up.

• Emergent surgical consultation should be obtained if evidence of generalized peritonitis.

Acute Pancreatitis

Risk Factors/Etiology

• The underlying etiology of pancreatitis is most commonly due to gallstones or alcoholism.

However the differential diagnosis is extensive.

• The presence of obstructing gallstones and cholangitis must be excluded as these

entitities represent surgical emergencies.

Clinical Presentation and Diagnoses

• The typical presentation of pancreatitis is epigastric pain radiating to the

back. Patients may also present with refractory vomiting and diffuse abdominal pain.

• Pancreatitis is a multisystem disorder which can lead to overwhelming organ failure

and death.

• Pulmonary: Hypoxemia, pleural effusions and pulmonary edema

• Cardiac: Tachycardia, hypotension and shock

• Neurologic: Confusion and coma

• Renal: Azotemia and oliguria

• Metabolic: Hypocalcemia, hyperglycemia, ketosis and hypertriglyceridemia

• Ranson’s criteria indicators of morbidity and mortality:

• 0-2- 2% mortality, 3-4- 15%, 5-6- 40%, 7-8- 100%

• Criteria on admission:

• age >55 yr

• white blood cell count >16000 IU/L

• blood glucose >200 mg/d

• serum LDH >350 IU/L

• SGOT >250 IU/dL

• At 48 h

• Hematocrit fall >10%

• BUN increase >8 mg/dl

• Arterial PO2 <60 mm hg

• Base deficit >4 meq/L

• Fluid sequestration >6 L

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• Lipase has higher diagnostic accuracy and is more cost effective compared to amylase.

Amylase is both of salivary and pancreatic origin, but most labs do not differentiate

between the two. Therefore the results of an elevated amylase are misleading. Lipase

has a higher sensitivity.

• Imaging studies are indicated in patients with intrabdominal sepsis and to rule out

complications. CT scan and ultrasound can be used. If suspect pancreatitis but no lab

diagnosis may be indicated.

Treatment

• Patients with pancreatitis may have baseline hypoxemia which progresses to ARDS if

not managed early. Once ARDS develops, pancreatic injury is exacerbated. Therefore

application of oxygen early on is preferred.

•. Caution should be used with administration of insulin as there is exaggerated response

with pancreatitis and profound hypoglycemia may result.

• These patients tend to be hypocalcemic and may benefit from supplementation.

• Nasogastric suction is no longer recommended as it prolongs hyperamylasemia and

increases pain medication requirement. However, it may be necessary in the case of

duodenal obstruction. Cimetidine, glucagon and atropine fail to show any benefit in

alleviating symptoms or complications.

• Patients will require admission and monitoring for complications such as pseudocyst,

gastrointestinal bleeding, cholangitis, ARDS, metabolic disturbances, encephalopathy

and DIC.

• CT scanning in patients with overwhelming sepsis without a source may identify cases

of pancreatitis. Autopsy studies have shown many missed cases of fatal pancreatitis in

this subgroup of patients.

• Mild cases without evidence of biliary tract involvement or systemic involvement may

be candidates for outpatient management if close follow-up is available.

Peptic Ulcer Disease and Gastritis

Risk Factors/Etiology

• H. pylori (most common cause of ulceration)

• NSAIDs, aspirin common cause of bleeding ulcers and gastritis

• Alcohol

• Bile reflux

• Pancreatic enzyme reflux

• Gastrinoma (Zollinger-Ellison syndrome)

• Severe stress (e.g., trauma, burns)

Clinical Presentation and Diagnosis

• Gastritis and PUD usually are indistinguishable in the ED without endoscopy.

• Typically epigastric/left upper quadrant burning pain that may radiate to the back

after meals.

• May be relieved by food, antacids (duodenal), or vomiting (gastric).

• A type and cross match should be sent if the patient is actively bleeding.

• Helicobacter testing is useful in the primary care setting to guide treatment.

Treatment

• Iced saline lavage should never be performed. This is a dangerous action. It had been

thought that cooling would cause vasoconstriction and accelerate cessation of bleeding,

but this is now known to cause arrhythmias without decreasing bleeding.

• Nasogastric tube. While evacuation of blood from the gut may be one benefit from

nasogastric lavage, this procedure can cause great discomfort. It may also be

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nondiagnostic in a large number of cases, and ultimately the patient will need endoscopy.

Therefore early consultation with the gastroenterologist is key.

• Etiology of gastrointestinal bleeds on endoscopy in those with history of varices found

the majority of patients with bleeding were bleeding from acute gastric duodenitis

followed by gastric ulcer then duodenal ulcer, varices, Mallory Weiss, esophagitis.

H2 Blockers and Proton Pump Inhibitors

• Proton pump inhibitors and H2 blockers are not effective in the acute phase of bleeding.

However proton pump inhibitors may help decrease rebleeding after endoscopy.

Vasoconstrictors

• Vasopressin not too beneficial and risk of hypertension, stroke, coronary ischemia

• Dose-related decrease in coronary flow and cardiac output

• Octreotide has a similar mechanism as somatostatin but is more potent and longer

acting decreasing splanchnic blood flow and inhibiting gastric acid secretion

• Patients required less blood transfusion, fewer required surgical and endoscopic intervention

after a 100 mcg bolus followed by 25 mcg/h when compared to H2 blockers

• Given to patients with hematemisis and/or tarry stool and evidence of bleeding peptic

ulcer on early endoscopy—subset to which it is applicable

Outpatient Management of UGI

Low risk criteria that have been identified that may warrant outpatient management:

• No high risk endoscopic feature/varices/portal hypertenisve gastropathy

• No debilitation

• No orthostatic vital sign change

• No liver disease or concomitant disease

• No anticoagulation or coagulopathy

• No fresh hematemesis

• No severe anemia

• Adequate home support

High Risk Criteria

• BLEED criteria good screening tool to decide which groups are likely to develop

related in-hospital complication. Bleeding, Low systolic blood pressure, Elevated prothrombin

time, Erratic mental status, Disease comorbid.

• 33% of patients with BLEED criteria had complications.

• Patients with an upper gastrointestinal bleed with signs of hypoperfusion such as

syncope, confusion, dizziness or hypotension should have myocardial ischemia excluded.

• Upper GI bleed

• Peptic ulcer disease:

• Risk groups include alcohol use, cigarette use, medications such as NSAID use.

• Variceal bleeds:

• Risk groups include those with liver failure and portal hypertension.

• Variceal bleeds are frightening but remember that most UGI bleeds in patients

with varices are from sources other than the varices.

• If do have variceal bleed, drug therapy to decrease splanchnic flow is first line therapy

(vasopressin and octreotide):

• Vasopressin decreases cardiac output, increases systolic hypertension, arrhythmias

and bradycardia. inhibits fibrinolysis and may therefore interfere with hemostasis.

• Requires a continuous infusion due to short half life (20 min)

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• Somatostatin is more effective in many regards—localized to splanchnic vasculature

and produces fewer effects but no difference in all cause hospital mortality

• When compared, long acting vasopressin and somatostatin (octreotide) equivalent

• Given the longer half life of octreotide and fewer adverse risks then may be better

• In last abstract initial control of bleeding achieved in 90% of patients with sclerotherapy

and 84% octreotide group

Massive GI Hemorrhage Treatment

Massive upper GI bleeding is a far more common emergency than lower GI bleeding.

It may present as hematemesis, melena or simply shock with a positive stool test

for blood or NG aspirate. Sources include peptic ulcer and gastroesophageal varices.

Massive lower GI bleeding is caused by angiodysplasia and diverticular disease.

Primary Survey Will Require Vigorous Suctioning of the Airway

• Wide open normal saline with multiple large bore IV’s (16 gauge or greater) are indicated

to treat shock. Type O blood should follow the first 2 L via rapid transfuser, until

type-specific and then cross-matched blood is available.

• Fresh frozen plasma is indicated for suspected coagulopathy (e.g., with stigmata of

chronic liver disease). NG tube for lavage and gastric emptying is indicated and may

be used as one gauge of active bleeding. Emergency endoscopy for hemostasis can be

performed by qualified personnel.

• In addition to emergent consultation for endoscopy, emergent surgical consultation

should be sought.

• Octreotide (50-100 mcg IV bolus followed by an infusion of 50 mcg/h) is indicated as

an adjunct to other therapies or when other therapies are unavailable for massive upper

GI bleeding.

• Balloon tamponade via Sengstaken/Blakemore or similar tube should be attempted in

the event of severe uncontrolled upper GI hemorrhage.

• Apparent massive lower GI hemorrhage may be from an upper GI source (which may

be revealed by NG tube or upper GI endoscopy).

• If these are negative, either interventional radiological methods or laparotomy will be

required to stop bleeding.

• Although not entirely reliable in acute hemorrhage, serial bedside hemoglobin determinations

are helpful in guiding resuscitations.

• Hypothermia should be avoided by covering the patient with warm blankets and using

warmed IV fluids and blood products.

• Stigmata of chronic liver disease as well as purpura and petechiae should be sought

on initial survey. This may assist in predicting the site of bleeding (e.g., the possibility

of esophageal and gastric varices) and need for factor replacement during the

resuscitation.

• A history of aortic repair surgery may indicate a aortoenteric fistula, which is managed

operatively.

Cholecystitis

Risk Factors/Etiology

• Common illness with over 15 million Americans affected.

• Present frequently for pain control.

• Typically in adult females. Tends to be associated with fatty meal. Incidence rises with

age. While uncommon in children, presence may suggest underlying disorder (sickle

cell, hemolytic anemia).

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Clinical Presentation and Diagnoses

• May present with abdominal pain in right upper quadrant or epigastrium which tends

to be constant and severe.

• Pain can radiate to shoulder or back.

• Nausea and vomiting common.

• Murphy’s sign: inspiratory arrest during palpation of RUQ.

• If fever or refractory pain is present or consider cholecystitis.

• Gallstones are either cholesterol (most common), pigment (associated with hemolytic

anemia).

• Elevated liver function studies suggest common duct obstruction, cholangitis, cholecystitis

or hepatic involvement.

• Ultrasound should be initial imaging study since it is over 90% sensitive and allows

visualization of common bile duct:

• Duct size over 10 mm suggests obstruction

• Gallbladder wall thickening over 5 mm or pericolic fluid suggestive of cholecystitis.

• HIDA scanning may detect obstruction or cholecystitis if stone is at neck of gallbladder

and nonvisualized on ultrasound.

• Routine abdominal films are of no utility.

Treatment

• The first priority is analgesia. NSAIDs have been used with great success. Narcotic

analgesics with antiemetic are also part of the initial therapy. Unsuccessful pain control

or cholecystitis needs hospital admission.

• Surgical consultation is required in patients requiring admission or those diagnosed

with cholangitis, common bile duct dilatation and/or cholecystitis.

• Antibiotics are indicated for acute cholecystitis, cholangitis, or common bile duct dilatation.

First line antibiotics include amp/sulbactam, flouroquinolone and flagyl or

pipercillin/tz.

Hernias

Risk Factors/Etiology

• A hernia occurs when a viscus internally or externally protrudes from its normal cavity.

• Risk factors include prematurity, family history, genitourinary abnormalities, ascites,

peritoneal dialysis, ventriculoperitoneal shunt, cystic fibrosis, lung disease, pregnancy,

or wound sites.

• Most hernias are inguinal and most occur in men.

• An indirect inguinal hernia occurs lateral to the inferior epigastric vessels. These are

the most common hernias in both men and women.

• A direct inguinal hernia is an acquired defect medial to the inferior epigastric vessels

and occurs mostly in older adults.

• A femoral hernia occurs below the inguinal ligament in the femoral canal, occurs

mostly in women, is very rare, and often becomes strangulated.

• An umbilical hernia occurs in infants. Most close spontaneously by one year of age.

• Spigelian hernias occur just lateral to the rectus sheath in the abdominal wall and are

very rare.

• A Richter hernia involves incarceration of the wall of a hollow viscus.

• An incisional hernia occurs at the site of a previous wound.

Clinical Presentation and Diagnosis

• An asymptomatic hernia presents without pain or tenderness, is reducible, and will

enlarge with standing or increased intra-abdominal pressure.

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• An incarcerated hernia is not reducible and is painful. It may or may not present with

symptoms of bowel obstruction, including nausea and vomiting.

• A strangulated hernia presents as a toxic appearing incarcerated hernia. Systemic toxicity

secondary to ischemic bowel may be present. If necrotic bowel is suspected do

not attempt to reduce the hernia and return the dead bowel into the abdomen.

• A femoral hernia will present with medial thigh and or groin pain.

• Diagnosis is based on clinical exam. Abdominal radiographs are useful to exclude a

bowel obstruction.

• A hernia must be distinguished from a scrotal hydrocoele, which will transilluminate

with a light source, while a hernia will not.

Treatment

• An incarcerated hernia without signs of bowel obstruction may be reduced with pain

meds and gravity and referred for surgical follow-up.

• Infants with inguinal hernias are at high risk for incarceration and should be urgently

referred to a pediatric surgeon for repair. In contrast, umbilical hernias often have a

benign course and do not require urgent referral.

• Strangulated hernias or any toxic-appearing patient should be started on broad spectrum

antibiotics, IV fluids, nasogastric decompression, and receive emergent surgical

consultation.

Esophageal Emergencies

Risk/Factors Etiology

• 75% of esophageal perforations are due to iatrogenic perforations.

• Boerhaave syndrome is the cause of 10% of esophageal perforations with 10% of these

due to trauma.

• Boerhaave syndrome occurs because the esophagus lacks a serosal layer, Thus, the wall

is weaker and may rupture at a lower intraluminal pressure, usually with severe vomiting.

Most perforations occurs in the lower third of the esophagus in the left posterolateral

region.

• All other cases of esophageal perforation are caused by foreign bodies or traumatic

perforations.

• Boerhaave syndrome is more common in middle-aged men after a drinking and eating

binge.

• Esophageal foreign bodies are most common in children. Most objects pass spontaneously.

The most common site of obstruction is the cricopharyngeal narrowing (C6).

Clinical Presentation and Diagnosis

• Delay in diagnoses of Boerhaave syndrome is common and leads to a high mortality

rate. Classic presentation for spontaneous rupture is vomiting followed by severe chest

pain. However, many patients have less dramatic presentations. Patients may present

with abdominal pain, dyspnea, and hematemesis.

• Subcutaneous emphysema may be palpable in the neck or chest. Hamman’s crunch

may be heard in 20% of cases over the heart. Patients usually appear acutely ill, hypotensive,

and septic depending on the delay in presentation.

• Esophageal foreign bodies usually present in adults with retching, vomiting, coughing,

dysphagia or choking. In kids, common symptoms also include refusal to eat and stridor.

• Diagnosis of foreign body ingestion includes plain radiographs. Patients with foreign

body sensation and negative radiographs should undergo direct laryngoscopy. Specialty

consultation should be obtained prior to contrast radiographs.

• Coins are visible on AP radiographs with the flat side visible if in the esophagus and on

end if in the trachea.

GI Emergencies 133

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Treatment

• Treatment of Boerhaave syndrome or a delayed iatrogenic perforation in the emergency

department includes rescusitation of shock, broad spectrum antibiotics, and

emergent surgical consultation.

• Esophageal foreign bodies require emergent surgical consultation if the patient appears

toxic, has an acute abdomen, bloody stools, or persistent vomiting.

• Button battery ingestion requires emergent GI consultation as esophageal burns can

occur within 4 h and perforation within 6 h.

• Food impaction can be treated conservatively if the patient can tolerate their own secretions.

Intravenous glucagon, 1 mg, can be used to relax esophageal smooth muscle.

Sublingual nitroglycerin can be used to relax lower esophageal sphincter pressure.

Anal/Rectal Disorders

Risk Factors/Etiology

• Hemorrhoids are more common in pregnancy and are associated with constipation

and straining bowel movements, obesity, and chronic liver disease. Internal hemorrhoids

are located above the dentate line and are painless. External hemorrhoids are

located below the dentate line and are painful.

• Anal fissures are the most common cause of painful rectal bleeding.

• Pilonidal cysts usually occur in young people and are a chronic recurring reaction to

an ingrown hair.

• Perirectal and perianal abscesses are common in diabetics and drug abusers.

Clinical Presentation and Diagnoses

• Internal hemorrhoids cause painless bright red blood with defecation. They are only

visible through an anoscope.

• External hemorrhoids cause pain with defecation and are usually visible on exam.

• Rectal bleeding must be referred for further evaluation for malignancy.

• Other causes of rectal pain include foreign body, venereal proctitis, trauma, abscesses,

and anal fissures.

• Anal fistulas present with malodorous bloody discharge through the fistula.

• Anal fissures present with painful bowel movements, with the pain resolving between

bowel movements.

• Perianal and perirectal abscesses present as a tender red mass and may have concurrent

fever and leukocytosis.

Treatment

• Most hemorrhoid patients may be managed conservatively with sitz baths, good hygiene,

bulk laxatives, and stool softeners. Thrombosed external hemorrhoids should

be referred to a surgeon, or may be excised and the clots removed in the ED if conservative

measures have failed.

• Surgical referral is needed for anal fistulas.

• Anal fissures may be treated conservatively with sitz baths and local analgesics.

• All but the most simple perianal abscesses should be drained and followed by a surgeon.

Perianal abscesses should be drained and packed, with antibiotics only necessary

in diabetics and other immunocompromised hosts.

• Most rectal foreign bodies can be removed in the ED after adequate analgesia. Antibiotics

and surgical or gastroenterological consultation should only be obtained in cases

of high risk or perforation or with peritoneal or other toxic signs.

• Pilonidal cysts may be drained and packed in the ED, with surgical referral appropriate

for definitive removal of the cyst.

134 Emergency Medicine

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Special Considerations

Elderly Patients with Abdominal Pain

Elderly patients presenting with abdominal complaints warrant a complete evaluation.

• Up to 50% of those over 65 yr of age will ultimately have a process evolving that

requires medical or surgical intervention. Therefore, it is judicious to check laboratory

and imaging studies.

• While physical examination is important, elderly patients frequently present atypically.

They will often lack fever and leukocytosis. For instance, it is well documented

that elderly patients will have perforated appendicitis at an early time and with a less

obvious exam, than their younger counterparts. Higher morbidity and mortality from

higher rates appendiceal perforation is the rule. After 50 yr of age perforation rates are

from 32-70%!

Delays in the diagnosis are typically due to:

• Atypical presentations

• Anatomy

• Less blood supply to appendix most likely

• One-third of perforations are in those with symptoms <24 h.

Additionally, the risk of solid masses increases as does the presence of

intra-abdominal infections. Elderly patients often will lack vital sign abnormalities.

They may have hemoperitoneum with normal vital signs.

HIV and Abdominal Pain

The immunosuppression of HIV creates diagnostic challenges. All the usual etiologies

should be considered such as appendicitis, cholelithiasis or nephrolithiasis.

However, there are a few unique considerations.

Medication related etiologies of abdominal pain in this group include pancreatitis,

acalculous cholecystitis and nephrolithiasis.

Immunosuppressive complications of their illness may include infection of the

biliary tract with M.A.I. or abdominal lymphomas or Kaposi’s sarcoma. They may

also present with parasitic infections such as amebiasis and liver cysts.

The syndrome of HIV diarrhea is common and a chronic condition. They may

also develop CMV infection through the gastrointestinal tract and have perforation.

Suggested Reading

1. American College of Emergency Physicians. Clinical Policy: Critical issues for the initial

evaluation and management of patients presenting with a chief complaint of nontraumatic

acute abdominal pain. Ann Emerg Med October 2000; 36:406-415.

2. Rao PM, Rhea JT, Novelline RA et al. Helical CT techniques for the diagnoses of appendicitis:

Prospective evaluation of a focused appendix CT examination. Radiology 1997;

202:139-144.

3. Albu E, Miller BM, Choi Y et al. Diagnostic value of a C-reactive protein in acute

appendicitis. Dis Col Rect 1994; 37(1):49-51.

4. Ramsden WH, Mannion RA, Simpkins KC et al. Is the appendix where you think it is—

and if not, does it matter? Clin Radio 1993; 47(2):100-103.

5. Lyons D, Waldron R, Ryan T et al. An evaluation of the clinical value of the leukocyte

count and sequential counts in suspected acute appendicitis. Br J Clin Pract 1987;

41:794-796.

6. Nase HW, Kovalcik PH, Cross GH. The diagnoses of appendicitis. Am Surg 1980;

46:504-507.

GI Emergencies 135

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7. Wagner JM, McKinney WP, Carpenter JL. Does this patient have appendicitis? JAMA

1996; 276:1589-1594.

8. Colucciello SA, Lukens TW, Morgan DL. Assessing abdominal pain in adults: A rational

cost-effective, and evidence-based strategy. Emergency Medicine Practice 1999; 1:1-16.

9. Trott AT, Lucas RH. Acute abdominal pain. In: Rosen, ed. Emergency Medicine Concepts

and Clinical Practice. 4th ed. 1998:1888-1901.

10. Greenfield RH, Henneman PL. Disorders of the small intestine. In: Rosen, ed. Emergency

Medicine Concepts and Clinical Practice. 4th ed. 1998:2005-2019.

11. Bitterman RA. Disorders of the large intestine. In: Rosen, ed. Emergency Medicine Concepts

and Clinical Practice. 4th ed. 1998:2027-2030.

CHAPTER 6

Emergency Medicine, edited by Sean Henderson. ©2006 Landes Bioscience.

Genitourinary Emergencies

Chi Lee, Sean O. Henderson and Sabrina Grassl

Urinary Tract Infections

• Urinary tract infections (UTIs) are one of the most frequently encountered infectious

processes diagnosed by emergency physicians (EPs). The epidemiology of UTIs varies

with sex and age.

• It is estimated that women have about a 50% lifetime occurrence rate for a UTI.

• The prevalence of UTIs in febrile infants is about 5%, while in the geriatric population

the prevalence approaches 20%.

• While the diagnosis of UTI is relatively straightforward, the treatment and ultimate

disposition of patients depends on special circumstances such as extremes of age,

pregnancy, treatment failures, and underlying medical conditions.

• UTIs are most often caused by Gram-negative aerobic bacilli, the most common of

these being E. coli in 80% of cases.

• The second most common pathogen (10-20%) is Staphylococcus saprophyticus, a

coagulase-negative Gram-positive bacteria.

• Proteus mirabilis, Klebsiella, and Enterococcus account for <5% of the remaining

infections.

Clinical Presentation

• Classically the signs and symptoms of lower UTIs are dysuria, frequency, urgency,

hesitancy, hematuria, and suprapubic pain.

• Upper UTIs (pyelonephritis) typically present with fever, chills, flank pain, nausea,

vomiting, anorexia, and associated costovertebral angle (CVA) tenderness.

• Some studies have shown that up to 50% of women with classical lower UTI symptoms

have silent kidney involvement.

• In women, a history of vaginal discharge should always be elicited, and a pelvic exam,

if indicated, will allow one to rule out PID, cervicitis, or vaginitis as the cause of

dysuria.

• Males with dysuria and discharge should undergo a urethral swab, which should be

sent for gonorrhea and chlamydia cultures.

Diagnosis

• The diagnostic mainstay of a UTI is the urinalysis (UA).

• A UA from a properly obtained midstream, clean-catch specimen is as accurate as

that of a catheterized specimen, except in debilitated patients, patients of extreme

ages, or the morbidly obese. For such patients, a catheterized specimen may be

necessary.

• An initial screening test is the urine dipstick. Leukocyte esterase (LE) and nitrites may

be present in UTIs.

• The urine dipstick for LE has a reported sensitivity of 75-96% with a specificity of

94-98% in detecting >10 leukocytes per high-powered field.

• The nitrite test detects the presence of bacteria that produce nitrite reductase and is

highly specific (92-100%) but not nearly as sensitive (35-85%).

Genitourinary Emergencies 137

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• Empiric treatment is appropriate in symptomatic patients with a positive LE test.

• If the urine dipstick is negative, urine microscopy is not indicated.

• Although direct microscopy techniques lack standardization, it is presently accepted

that the presence of 8 leukocytes or more per mL of uncentrifuged urine constitutes

pyuria.

• In a patient with pyuria without bacteriuria, the diagnosis of sexually transmitted

urethritis should be considered.

• Microscopic hematuria is more commonly caused by a UTI than a sexually transmitted

disease (STD).

• In patients with pyelonephritis the UA will often show white blood cell casts.

• Most cases of uncomplicated UTIs do not necessitate a urine culture. But there are

several important risk factors for complicated UTI in which urine cultures should be

obtained. These include:

• All children, adult males, and debilitated elderly

• Immunosuppressed patients (HIV, steroid use, solid organ transplant patients)

• Pregnant women

• Treatment failures, recurrent UTIs, or previous antimicrobial therapy within 2 wk

• Hospitalized (or recently) patients

• Patients with chronic indwelling catheters or recent instrumentation

• Acute pyelonephritis

• Patients with preexisting anatomic urologic abnormalities or urinary tract obstruction

• Patients with serious medical diseases (DM, sickle cell anemia, cancer)

• Additional laboratory tests such as CBC, electrolytes, BUN and creatinine are optional,

and should be tailored to each individual.

• Blood cultures are of little value.

Differential Diagnosis

• For lower UTI:

• Urethritis

• Cervicitis

• PID/STDs

• Vulvovaginitis

• Prostatitis

• Epididymitis

• For upper UTI:

• All of the above

• Nephrolithiasis

• Renal abscess

• Appendicitis

• Cholecystitis

• Lower lobe pneumonia

• Diverticulitis

Special Circumstances

• Pyelonephritis

• Clinical presentation is classic lower UTI symptoms (dysuria, frequency, etc) with

associated CVA/flank pain, nausea, vomiting, dehydration or toxic appearance.

• Obtain urine culture in all cases. CBC is optional, and blood cultures are not indicated.

• Resuscitate early with 1-2 L of NS.

• Early parenteral antibiotics

• Antiemetics for vomiting, and analgesia for pain

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• Admission criteria

• Inability to tolerate oral intake (perisistent nausea/vomiting)

• Pregnancy

• Unstable vital signs and toxic appearance

• Immunocompromised state (diabetes, cancer, transplant, patient AIDS, sickle

cell disease)

• Any underlying anatomical urinary tract abnormality or obstruction

• Extremes of age

• Poor social situation or unreliable follow-up

• Pregnancy

• Asymptomatic bacteriuria (ASB) is defined as persistent colonization of the urinary

tract without UTI symptomatology.

• Untreated ASB is associated with increased incidence of preterm delivery and low

birth weight infants. The progression of ASB to pyelonephritis is associated with

significant maternal and fetal morbidity and mortality.

• About 5-10% of pregnant women will have ASB.

• ASB should always be treated with a 3-7 day course of oral antibiotics followed by

culture at the end of treatment to ensure sterilization of the urine.

• There is a paucity of literature on cystitis in pregnancy and its relationship to the

risk of preterm birth, low birth weight, or pyelonephritis.

• For cystitis, diagnosis can be obtained from urine culture. Treatment is the same as

that for ASB, but should be extended to 7-10 days. Patients should be have a repeat

urine culture done after treatment to ensure sterilization.

• Acute pyelonephritis occurs in 1-2% of all pregnancies. Clinical signs and symptoms

do not vary much from those of the nonpregnant population, but because of various

anatomic and physiologic changes during pregnancy, a broader differential diagnosis

must be considered. This includes normal back pain of pregnancy, gallbladder disease,

renal abscess, nephrolithiasis, pulmonary embolism, and appendicitis.

• Any evidence of renal involvement requires admission for IV antibiotics.

• Elderly

• 20-50% of women over 65 yr of age have ASB. The incidence increases with age

and is thought to be due to a combination of factors including changes in bladder

emptying, increased incontinence (both fecal and urinary), and decrease in estrogen

levels.

• The elderly often lack the usual presenting signs and symptoms. They may present

with fever, but hypothermia and euthermia are also not uncommon. The chief

complaint may be altered mental status, nausea and vomiting, weakness, dizziness,

abdominal pain, or respiratory distress.

• In general, ASB in the elderly is not treated. However, elderly patients presenting

with symptoms consistent with UTI, foul-smelling urine, or new symptoms of

urge incontinence should be treated.

• Acute pyelonephritis usually presents as a septic syndrome with fever, tachycardia

and altered mental status.

• Misdiagnosis of UTI in the geriatric patient is about 20-40% due to the wide range

of presenting symptoms.

• Men

• The incidence of bacteruria in the adult male is uncommon, but rises at the age of

50 with increasing incidence of prostatic hypertrophy. By age 65, the incidence of

UTIs among males and females becomes equal.

• UTIs in the male population are always considered complicated because the etiology

is usually due to a structural or functional defect, which leads to incomplete

voiding or obstruction.

Genitourinary Emergencies 139

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• The diagnosis of UTI in the male is made by urine culture. Physical exam can assist

in determining the cause as cystitis, prostatitis, or epididymitis.

• In males, a lower bacterial colony count (103-104 cfu/ml) is considered positive.

• Treatment is the same as that for women, but for the duration of 7-10 days. Nitrofurantoin,

however, is not recommended because it does not achieve reliable tissue

concentrations in the prostate.

• The presence of a UTI in males of any age warrants a genitourinary follow-up.

Treatment

• Treatment choice and duration is guided by several factors: anatomic localization of

infection (lower vs. upper UTI), severity of symptoms, and special considerations

mentioned above.

• Antibiotic selection should be guided by current and local resistance patterns to the

most common urinary pathogens. For instance, resistance to Trimethoprim/

Sulfamethoxazole (TMP/SMX) has been shown to be as high as 35% in parts of the

West Coast, while resistances to ciprofloxacin and nitrofurantoin are 1% and 13%

respectively.

• Adults

• Acute uncomplicated UTI

• TMP/SMX DS PO bid x 3 days

• Only in areas where resistance is <10%

• No history of recent hospitalization

• No recurrent UTI in the past year

• No recent use of TMP/SMX in the previous 6 mo

• Ciprofloxacin 250 mg PO bid x 3 days

• Levofloxacin 250 mg PO qd x 3 days

• Amoxicillin clavulanate 875 mg PO bid x 3 days

• Any oral cephalosporin x 3 days

• Other fluoroquinolones x 3 days

• Nitrofurantoin 100 mg PO bid x 7 days (caution in patients with G6PD deficiency)

• Fosfomycin 3 g single oral dose

• Treat dysuria with phenazopyridine 100-200 mg PO tid x 2 days, only. Warn

patients of orange color change in urine and contact lenses.

• Acute complicated UTI

• Ciprofloxacin (or other fluoroquinolone) x 7 days

• Acute uncomplicated pyelonephritis (outpatient)

• Ciprofloxacin 500 mg PO bid x 7 days (preferred)

• Levofloxacin 500 mg PO bid x 7 days

• Other fluoroquinolones for 7 days

• Acute uncomplicated pyelonephritis (inpatient)

• All treatment x 14 days. Treat with IV antibiotics until afebrile for 24-48 h, then

may be switched to oral meds for the remaining duration of therapy.

• Ciprofloxacin 400 mg IV bid

• Levofloxacin 250 mg IV qd

• Ceftriaxone 1-2 g IV qd

• Cefotaxime 1-2 g IV q 4-12 h

• Ampicillin 150-200 mg/kg/day IV divided q 4 h + gentamicin 5-7 mg/kg qd

• IV Pipercillin/tazobactam 3.375 g IV q 6 h

• Complicated pyelonephritis, urosepsis, and indwelling catheter

• Treatment duration 14 days

• Ciprofloxacin 400 mg IV q 8 h + gentamicin 5-7 mg/kg qd

140 Emergency Medicine

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• Ampicillin 150-200 mg/kg/day IV divided q 4 h + gentamicin 5-7 mg/kg qd

• Pipercillin/tazobactam 3.375 g IV q 6 h

• Ticarcillin/clavulinic acid 3.1 g IV q 6 h

• Imipenim 0.5 g IV q 6 h

• Pregnancy

• Cystitis/Lower UTI: (3-7 days)

• Amoxicillin

• Cephalexin

• Nitrofurantoin (increased risk of hemolytic anemia with G6PD deficiency)

• TMP/SMX (in areas with low resistance only, contraindicated in first and third

trimesters)

• Pyelonephritis: (10-14 days)

• Ampicillin + gentamicin

• Cephalosporins (cetazolin)

• Aztreonam

• TMP/SMX (contraindicated in first and third trimesters)

Emphysematous Pyelonephritis

• Emphysematous pyelonephritis (EPN) is a rare acute necrotizing parenchymal and

perirenal infection caused by gas-forming uropathogens, namely E. coli, K. pneumonia,

and Proteus spp.

• The condition predominantly affects diabetic patients, with high tissue glucose levels

providing the substrate for carbon dioxide-producing microorganisms.

• EPN preponderantly affects females over males (6:1), which may be due to the increased

susceptibility to UTI in females, and all the documented cases of emphysematous

pyelonephritis have been in adults.

• The left kidney is more commonly affected than the right, reflecting the preponderance

of left-sided urinary tract obstruction.

Clinical Presentation

• The most common presentation of EPN is fever, flank pain, and pyuria, a clinical

picture not significantly different from a classic upper UTI.

• Thrombocytopenia, acute renal function impairment, disturbance in consciousness,

and shock can be initial presentations.

• The overall mortality is described to be around 40%, with delay in diagnosis and

treatment contributing to both morbidity and mortality.

Predictors of Outcome

• The most reliable predictor of outcome in EPN has been determined to be serum

creatinine.

• Patients with serum creatinine levels >1.4 mg/dl had an increase in post-test probability

of death from 69-92% in one study.

• Platelet counts 60,000/mm or less also indicated higher risk of mortality.

• Additionally, disturbance of consciousness and shock are associated with mortality

and poor outcome, explained by expected poor prognosis of CNS and cardiovascular

dysfunction.

Diagnosis

• The diagnosis of EPN is classically made by demonstrating the presence of gas in renal

or perinephric tissue by plain abdominal X-ray film or by renal ultrasound.

• When present, a crescent shaped collection of gas over the upper pole of the kidney is

more distinctive than mottled gas shadows, which are often mistaken for bowel gas.

Genitourinary Emergencies 141

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• As the infection progresses, gas extends into the perinephric space and retroperitoneum.

However, gas could be demonstrated only on one-third of plain abdominal radiographs

in some studies.

• Ultrasonography usually demonstrates strong focal echoes, suggesting the presence of

intraparenchymal gas; however, it may again be difficult to distinguish the necrotic

gas-filled area from gas in the bowel. IVP is rarely of value as the affected kidney

usually is nonfunctioning or poorly functioning.

• Obstruction has been demonstrated in approximately 25% of EPN cases.

• CT scan is the best means to localize gas and extent of infection.

• The presence of streaky or mottled gas with or without bubbly and loculated gas

appears to be associated with rapid destruction of renal parenchyma and a 50-60%

mortality rate.

• A gas pattern characterized by the presence of bubbly or loculated gas and the

absence of streaky or mottled gas is associated with a more favorable prognosis.

• A renal CT scan should be performed to assess the degree of renal function impairment

of the involved kidney and the status of the contralateral kidney.

Management

• Patients should be started on appropriate antimicrobial agents, and treatment of diabetes

must be initiated.

• Obstruction of the affected kidney, if present, must be eliminated, and function of the

contralateral kidney must be established, because of reported bilateral cases.

• At the same time, surgical intervention poses a substantial risk for patients with hemodynamic

instability caused by fulminant infection and is not an appropriate option for

bilateral kidney involvement.

• Previous studies have emphasized that surgical treatment must be complete extirpation.

In more recent studies, CT-guided percutaneous drainage has proven successful

in as high as 92% of patients in treating multiloculated, ill-defined, and extensive

dissecting air and fluid collections in EPN, with 80% nephron-sparing.

Perinephric Abscess

• Perinephric abscess is a life-threatening but treatable process, consisting of suppurative

material occupying the space between the renal capsule and the surrounding fascia.

• Most of the perinephric abscesses result from the rupture of an intrarenal abscess into the

perirenal space, and are caused most commonly by E. coli, Proteus species, and S. aureus.

• Other sources include dissemination from other sites of infection including liver, gallbladder,

pancreas, pleura, prostate, and the female reproductive tract.

• Much of the associated mortality is the result of failure to diagnose this entity in a timely

fashion. This failure may be due to the nonspecific clinical picture on presentation.

Clinical Features

• The symptoms of perinephric abscess, including fever, flank pain, chills, nausea, vomiting,

and dysuria, may develop insidiously, making early recognition difficult.

• Fever is the most common symptom

• Abdominal tenderness

• Referred pain is also common to areas of the hip, thigh, and knee.

• The peripheral white blood cell count is usually elevated with a left shift.

• Urinalysis may be normal up to one-third of the time, and blood cultures as well as urine

cultures may fail to identify correctly the bacterial pathogens responsible for the abscess.

• Distant extension of a perinephric abscess may result in a multitude of processes including

empyema and colon perforation. While these extensions are rare, direct extensions

into the flank or psoas muscles are more common, which may even extend to

drain as a flank abscess.

142 Emergency Medicine

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Diagnosis

• A perinephric abscess should be in the differential of patients presenting with fever of

unknown origin and with unexplained peritonitis, pelvic abscess, or empyema.

• Additionally, perinephric abscess should be considered in the differential diagnosis of

any patient presenting with a urinary tract infection that fails to respond promptly to

antibiotic therapy, particularly in those known to have anatomical abnormalities of

the urinary tract or diabetes mellitus.

• Chest X-ray and abdominal films may show a range of findings, including subtle

abnormalities, nonspecific findings, or nothing at all.

• Ultrasonography, however, will show a mass, often with thickened, uneven walls, with

heterogeneous internal echoes. However, the ultrasound was falsely negative in as high

as 36% of cases when compared to CT in one study. CT scan, therefore, is the diagnostic

test of choice as it identifies the abscess and defines involvement of surrounding

and distant structures.

Treatment

• Perinephric abscesses have been associated with mortality rates as high as 50%, although

with early recognition by CT scan, prompt percutaneous drainage, and effective

antimicrobial therapy, mortality has decreased.

• Unlike intrarenal abscesses, antibiotic therapy alone is not sufficient in treating perinephric

abscesses.

• Percutaneous drainage under CT or ultrasound guidance with adjunctive antibiotics

is recommended as the treatment of choice.

• If percutaneous drainage fails or is contraindicated, surgical drainage is performed.

• Empiric antimicrobial therapy should be directed mainly against common

Gram-negative uropathogens and S. aureus.

• An aminoglycoside (gentamicin or tobramycin) and an anti-staphylococcal ²-lactam

(oxacillin, nafcillin, cefazolin) are appropriate initial antibiotics.

• An extended spectrum ²-lactam may be used in place of an aminoglycoside for

Gram-negative coverage in case of abnormal renal function.

• Once cultures are done, antibiotic therapy should be modified accordingly.

Renal Abscesses

• Intrarenal abscesses are classified into renal cortical abscess and renal corticomedullary

abscess.

• The treatment of renal abscesses is still under debate, perhaps because of the failure of

many recent studies to distinguish between renal cortical abscesses and renal corticomedullary

abscesses, which are different in their pathogenesis, prognosis, and therapies.

• Similar to perirenal abscesses, patients with intrarenal abscesses can present to the

Emergency Department acutely with fever, flank pain, nausea, and vomiting, masking

as a classic pyelonephritis. However, mortality rate for intrarenal abscess has been

positively correlated with the timeliness of diagnosis.

Renal Cortical Abscess (Renal Carbuncle) vs Renal Corticomedullary

Abscess

Pathogenesis

• Renal carbuncles result from hematogenous spread of bacteria from primary focus of

infection elsewhere in the body, usually skin lesions such as cutaneous carbuncles,

furuncles, paronychia, cellulitis, osteomyelitis, and endovascular infections.

• The most common cause is S. aureas infection, and conditions associated with an

increased risk for staphylococcal bacteremia such as diabetes mellitus and intravenous

drug use are predisposing factors.

Genitourinary Emergencies 143

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• Most carbuncles are unilateral, single lesions occurring in the right kidney. Only 10%

of these eventually rupture through the renal capsule to form a perinephric abscess.

• In contrast, renal corticomedullary infections occur most commonly as a complication

of ascending urinary tract infections with or without accompanying urinary tract

abnormalities, which include most commonly obstructive problems such as scarring

from previous infections or renal stones, or genitourinary abnormalities associated

with diabetes mellitus.

• Enteric aerobic Gram-negative bacilli, including Escherichia coli, Klebsiella species, and

Proteus species are commonly responsible for renal corticomedullary infections.

• Another contrast between renal cortical abscesses and renal corticomedullary abscesses is

that the Gram-negative corticomedullary infection frequently causes a severe parenchymal

infection that may extend to and perforate the renal capsule, thus more commonly

forming a perinephric abscess.

Clinical Features

• Unlike other intrarenal abscesses, renal carbuncles are approximately three times more

common in men than in women.

• They occur most commonly between the second and fourth decades of life in patients

presenting with chills, fever, back or abdominal pain, and few localizing signs.

• Although 95% of patients present with elevated white blood cell counts, most patients

do not have bacteruria or dysuria as the infectious process is circumscribed in the

cortex and generally does not communicate with the excretory passages.

• Consequently, urinalysis is usually normal. Likewise, blood cultures are usually negative.

• Although dysuria may not necessarily be present in renal corticomedullary patients,

they may have a previous history of recurrent urinary tract infections, renal calculi, or

a history of prior genitourinary instrumentation.

• Again, leukocytosis is generally present, but urinalysis is often abnormal in renal

corticomedullary abscesses (70% of the time) with bacteriuria, pyuria, proteinuria, or

hematuria because of drainage into the collecting system.

Diagnosis

• The nonspecific clinical presentation of fever, chills, and back pain may be seen with a

variety of renal processes.

• Renal cortical abscesses can mimic renal tumors, cysts, renal corticomedullary abscesses,

and perirenal abscesses. Furthermore, renal cortical abscesses are difficult to

distinguish from renal medullary abscesses.

• Ultrasonography is useful in the diagnosis of cortical abscesses because it provides

information about renal morphology and characterizes an intrarenal lesion as cystic,

tumorous, or suppurative.

• Furthermore, the ultrasound can provide information about the presence of an

obstructive uropathy, retroperitoneal or intra-abdominal processes, and suppurative

renal complications .

• Although the ED ultrasound is used often to diagnose patients with intrarenal abscess,

there are no current studies that describe the sensitivity and specificity of its

use in the ED.

• To date, the CT scan provides the most anatomic information and is able to detect

abscesses <2 cm in size.

• Particularly if the ultrasound is equivocal or negative, CT scan may be of benefit in

definitive diagnosis.

• On CT, most abscesses appear as low-density masses with vascular enhancement of

the wall. Gas within a low-density mass is pathognomonic for an abscess.

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Prognostic Factors

• Bamberger et al demonstrated that poor prognostic factors were abscesses of diameter

>5 cm, involvement by more than one organism, presence of Gram-negative bacilli,

duration of therapy <4 wk, and use of aminoglycoside as the only antibiotic.

• Factors that bear resistance to antibiotic therapy alone include large abscesses, renal

obstruction, advanced age, and urosepsis.

Treatment

• Unlike emphysematous pyelonephritis, renal abscesses are managed medically as firstline

treatment.

• There is mounting evidence that the success of renal abscesses treated with antibiotics

alone can be as high as 86% in large studies. Because S. aureus is usually the cause of

the renal carbuncle, it responds to antistaphylococcal antibiotics, and surgical intervention

is not required.

• If urinalysis shows no bacteria or Gram-positive cocci, oxacillin or nafcillin, 1-2 g

every 4-6 h, is the therapy of choice.

• For penicillin allergic patients, first generation cephalosporins provide adequate

Gram-positive coverage.

• Parenteral antibiotics should be continued for 10 days to 2 wk, and subsequent oral

antistaphylococcal therapy for 2-4 wk.

• The course of resolution includes defervescence after 5-6 days of IV antibiotics,

and improvement of flank pain in <24 h.

• For renal corticomedullary abscesses, medical therapy is successful in most cases; however,

smaller renal abscesses are more successfully treated with antibiotic treatment

alone than larger abscesses, >5 cm in diameter.

• In most cases, an intensive trial of appropriate antibiotic therapy should be attempted

before considering surgical drainage for lesions localized to the renal parenchyma.

• Antimicrobial therapy should target the most common bacterial organisms, including

E.coli, Klebsiella, and Proteus species.

• Monotherapy can be given with an extended spectrum penicillin, and extended

spectrum cephalosporin or ciprofloxacin. Combination therapy has not been proven

to be any more effective.

• Considerations for the ED physician in determining whether further surgical intervention

is needed include failure of antibiotic therapy, large abscess >5 cm diameter,

multifocal abscesses, obstructive uropathy, advanced age, deteriorating patient, and

immunocompromised patient.

• Percutaneous drainage of the abscess combined with full course of parenteral antibiotics

have been shown to be successful in those requiring drainage, offering the advantages

of minimal invasiveness, favorable nephron-sparing, and minimal morbidity.

• If open drainage is required, incision and drainage, not total nephrectomy, are recommended

when possible.

• Nephrectomy is reserved for elderly, septic patients with diffuse renal parenchymal

injury requiring urgent intervention for survival.

Nephrolithiasis

• Urologic stone disease is one of the most common disorders of the urinary tract, and

one of the most common diseases seen in the ED.

• About 2-5% of the population will form a urinary stone during their lifetime.

• Several factors correlate with an increased incidence of stone formation: men greater

than women (3:1 ratio), age between 20 and 50 yr, a sedentary lifestyle, warm weather

(peak incidence during the hottest 3 mo) and residence in the Southeastern United

States.

Genitourinary Emergencies 145

6

• In addition, there is increased genetic predisposition seen within families.

• Nephrolithiasis is a recurrent disease for most people with 37% developing another

stone within 1 yr, 50% within 5 yr, and 70% within 9 yr.

• There are four basic types of renal stones (Table 6.1):

• calcium

• struvite

• uric acid

• cystine

• Retrieval and subsequent analysis of the stone is important to determine possible causes

of stone formation and guide future therapy.

Clinical Presentation

• The classic presentation of renal colic is a history of abrupt onset of severe, crescendo

flank pain that eventually radiates into the lower abdomen and ipsilateral testes or

labia as the stone progresses down the ureter.

• The patient is often found writhing in bed, unable to find a comfortable position.

• This is in marked contrast to the patient with peritonitis who will be lying completely

still avoiding any movements.

• The pain is colicky in nature, waxing and waning, but rarely absent.

• Nausea and vomiting are almost always present, and abdominal distension with an

ileus is not uncommon.

• A history of fevers or chills is suggestive of infection and should be aggressively

pursued.

• About one-third of patients will give a history of gross hematuria.

Diagnosis

• The most important laboratory test to obtain in this clinical setting is the urinalysis.