Emergency And Acute Medicine - Glaucoma


Basics Description
Glaucoma is a group of disorders characterized by elevated intraocular pressure, progressive optic neuropathy, and irreversible vision loss if untreated.


Etiology
Primary glaucoma includes open-angle and angle-closure forms. Primary open-angle glaucoma has a normal anterior chamber angle, insidious onset, and chronic elevation of intraocular pressure. It accounts for approximately 90% of glaucoma cases in the United States and is a leading cause of blindness in African Americans. Risk factors include African American race, age over 40 years, family history, myopia, diabetes, and hypertension.
Primary angle-closure glaucoma results from narrowing or closure of the anterior chamber angle, preventing normal aqueous humor outflow through the trabecular meshwork. It presents abruptly with a sudden rise in intraocular pressure. Risk factors include Asian and Eskimo ethnicity, hyperopia, increasing age, female sex, and family history.
Secondary glaucoma may be open or closed angle and occurs due to other conditions such as ocular disease, trauma, systemic illness, or medications. Common drug causes include steroids, sertraline, bronchodilators, and topiramate. Associated diseases include uveitis, neovascularization, neurofibromatosis, intraocular tumors, trauma, and rapid correction of hyperglycemia.


Diagnosis Signs And Symptoms
Open-angle glaucoma typically causes painless, gradual loss of peripheral vision and may present late. Angle-closure glaucoma classically presents with painful loss of vision and a fixed, mid-dilated pupil.
History in open-angle disease includes slow bilateral visual decline or night blindness without pain. Angle-closure disease presents with severe eye pain, ipsilateral headache, nausea, vomiting, decreased visual acuity, halos around lights, and visual clouding. Symptoms may be triggered by dim lighting or medications such as anticholinergics, sympathomimetics, antihistamines, antipsychotics, tricyclic antidepressants, and sulfonamides like topiramate.
Physical examination in angle-closure glaucoma reveals decreased visual acuity, a mid-dilated nonreactive pupil, corneal edema with hazy appearance, conjunctival injection with ciliary flush, and a firm globe on palpation.


Essential Workup
A complete ocular examination is required, including visual acuity testing, tonometry, and slit-lamp examination.


Diagnosis Tests And Interpretation
Normal intraocular pressure ranges from 10–21 mm Hg. In open-angle glaucoma, pressure elevation is variable and may be normal in up to 30% of patients. In angle-closure glaucoma, any elevation is abnormal and values are often greater than 40 mm Hg. Slit-lamp examination evaluates the anterior chamber and excludes other ocular pathology. Gonioscopy provides direct assessment of the chamber angle and confirms angle closure.


Differential Diagnosis
Cavernous sinus thrombosis, acute iritis or uveitis, retinal artery or vein occlusion, temporal arteritis, retinal detachment, conjunctivitis, and corneal abrasion.


Treatment Pre Hospital
No specific prehospital ocular intervention is required. Provide analgesia as needed and stabilize other injuries if trauma is involved.


Initial Stabilization Therapy
In suspected acute angle-closure glaucoma, immediately initiate measures to reduce intraocular pressure and discontinue precipitating medications when applicable.


Ed Treatment Procedures
Open-angle glaucoma requires recognition and urgent ophthalmology referral. Long-term management typically involves topical beta-blockers or prostaglandin analogs.
Acute angle-closure glaucoma is an ophthalmologic emergency. Immediate treatment includes topical beta-blockers and alpha-2 agonists to reduce aqueous humor production, carbonic anhydrase inhibitors such as acetazolamide, and hyperosmotic agents like mannitol in severe cases. Once intraocular pressure is below 40 mm Hg, pilocarpine is used to constrict the pupil and open the trabecular meshwork. Topical corticosteroids reduce inflammation. Emergent ophthalmology consultation is required for definitive management, often with laser iridectomy. Adequate analgesia and antiemetics should be provided.


Medication
Common agents include acetazolamide, mannitol, pilocarpine, prednisolone acetate, topical beta-blockers (timolol, betaxolol), alpha-agonists (apraclonidine, brimonidine), carbonic anhydrase inhibitors (dorzolamide, brinzolamide), and prostaglandin analogs (latanoprost, bimatoprost, travoprost). Prostaglandin analogs are first-line for open-angle glaucoma due to favorable side-effect profiles, though cost may limit use.


Follow-Up Disposition
Admission is indicated for severe pain, nausea, vomiting, need for parenteral therapy, or lack of improvement in intraocular pressure. Patients with symptom resolution and improved pressures may be discharged after ophthalmology evaluation with close follow-up within 24 hours.


Issues For Referral
If ophthalmology is unavailable, initiate treatment and transfer the patient to a facility with ophthalmologic services.


Follow-Up Recommendations
Open-angle glaucoma requires urgent outpatient ophthalmology follow-up. Angle-closure glaucoma requires immediate specialist intervention.


Key Clinical Insights And Avoidable Errors
Delayed reduction of intraocular pressure can lead to permanent vision loss. Eye pain or headache associated with abdominal symptoms should prompt ocular evaluation to avoid missed diagnosis. Patients using topical beta-blockers may develop systemic adverse effects such as bradycardia, hypotension, or syncope, which can complicate presentation and management.

Emergency And Acute Medicine - Giardiasis


Basics Description
Giardiasis is a noninvasive diarrheal illness caused by a protozoan parasite and is found worldwide. Prevalence ranges from 2–15% in developed countries and 20–40% in developing nations. It accounts for approximately 5% of travelers’ diarrhea and is the most common intestinal parasitic infection in the United States. Incidence peaks in early summer through fall, with highest rates in children aged 1–9 years and adults aged 30–39 years. Transmission occurs via the fecal–oral route. Humans are the primary reservoir, but domestic and wild mammals and contaminated surface water also serve as reservoirs. Populations at increased risk include travelers to endemic or wilderness areas, children in day care centers and their contacts, institutionalized individuals, and those engaging in anal sexual practices.


Etiology
Giardia lamblia is a flagellated protozoan, also known as Giardia intestinalis or Giardia duodenalis. After ingestion, organisms attach to intestinal villi and disrupt brush-border enzymes, leading to impaired digestion of lactose and other carbohydrates. No toxin is produced.


Diagnosis Signs And Symptoms
Symptoms typically begin 1–2 weeks after exposure. Infection is often asymptomatic. Symptomatic disease usually presents with acute-onset diarrhea that is foul-smelling, nonbloody, and frequently associated with steatorrhea. Illness is usually self-limited within 2–4 weeks but may be more severe in immunocompromised patients or those with underlying bowel disease. Common associated symptoms include flatulence, bloating, abdominal cramping, nausea, vomiting, malaise, anorexia, and weight loss. Fever is uncommon.
Thirty to fifty percent of patients develop chronic infection lasting longer than four weeks, characterized by fat malabsorption, secondary lactase deficiency, and macrocytic anemia due to folate deficiency. Pediatric patients may develop severe dehydration in acute disease and failure to thrive, growth retardation, or cognitive impairment in chronic infection. Physical examination is often benign. Extraintestinal manifestations include polyarthritis, urticaria, aphthous ulcers, maculopapular rash, and biliary tract disease.


Essential Workup
Evaluation should focus on exposure history, travel, high-risk group membership, and hydration status. The presence of gross or occult blood on rectal examination makes giardiasis unlikely.


Diagnosis Tests And Interpretation
Stool microscopy for ova and parasites has a sensitivity of 50–70% with one sample and up to 85–90% with three samples collected over several days. Specificity approaches 100%. Stool antigen detection by ELISA or immunofluorescent assay is highly sensitive and specific but does not detect other parasites. Stool PCR offers near-perfect sensitivity and specificity. Fecal leukocytes and stool cultures are unnecessary unless invasive bacterial infection is suspected. CBC may show macrocytic anemia in chronic disease. Electrolytes and renal function should be assessed if dehydration is present. Imaging studies are nonspecific and rarely required.


Differential Diagnosis
Viral gastroenteritis, bacterial enteritis, other protozoal infections, inflammatory bowel disease, irritable bowel syndrome, lactase deficiency, tropical sprue, medication or toxin-induced diarrhea, endocrine disorders, and gastrointestinal malignancy.


Treatment Initial Stabilization Therapy
Assess airway, breathing, and circulation. Administer intravenous isotonic fluids for significant dehydration. Children with severe dehydration require rapid fluid boluses and glucose monitoring.


Ed Treatment Procedures
Oral rehydration is sufficient for mild dehydration. Correct electrolyte abnormalities. Obtain stool studies when possible. If stool testing is negative but suspicion remains high, empiric treatment with metronidazole may be considered, and gastroenterology referral arranged for persistent symptoms.


Medication
First-line therapy includes metronidazole or tinidazole, each achieving cure rates near 90%. Metronidazole is given for 5–10 days, while tinidazole is administered as a single dose. Second-line agents include albendazole, nitazoxanide, quinacrine, paromomycin, or furazolidone when first-line therapy fails. Treatment choice should consider age, pregnancy status, renal function, and G6PD deficiency. Immunocompromised patients may require combination or prolonged therapy.


Follow-Up Disposition
Admission is indicated for patients with hemodynamic instability, severe electrolyte imbalance, inability to tolerate oral intake, or significant comorbid illness. Most patients can be discharged once hydration is adequate and symptoms are controlled.


Follow-Up Recommendations
Gastroenterology referral is recommended for persistent symptoms beyond four weeks despite therapy. Patients should be counseled regarding possible prolonged lactose intolerance and postinfectious fatigue.


Clinical Insights And Common Errors
Diagnosis is the primary challenge. Giardiasis should be considered in all patients with diarrhea, even without classic risk factors. A single stool specimen is often insufficient to exclude infection. Failure to recognize chronic disease and malabsorption can delay appropriate treatment.

Emergency And Acute Medicine - Giant Cell Arteritis (Temporal Arteritis)


Basics Description
Giant cell arteritis is a chronic vasculitis of large- and medium-sized arteries occurring almost exclusively in individuals older than 50 years. It is commonly referred to as temporal arteritis. The median age at onset is approximately 72 years. The disease most often involves arteries arising from the aortic arch. Although frequently clinically silent, thoracic aortic involvement is common and may lead to aneurysm or dissection. Thoracic aortic aneurysm occurs at a rate nearly 17 times higher than in those without giant cell arteritis, while abdominal aortic aneurysm is about twice as common.
Pathologic specimens demonstrate patchy mononuclear granulomatous inflammation with marked intimal thickening and luminal occlusion. Occlusive arteritis may involve the ophthalmic artery, resulting in anterior ischemic optic neuropathy and acute visual loss, which constitutes an ophthalmic emergency. Inflammation of arteries supplying the muscles of mastication causes jaw claudication and tongue discomfort.
Age is the greatest risk factor; the disease is rare in patients younger than 50 years and more than 90% of cases occur in those older than 60 years. Prevalence in individuals over 50 is approximately 1:500, with higher rates in northern latitudes. It is two to four times more common in women, rare in African American patients, and more common in White populations. There is a strong association with polymyalgia rheumatica, present in approximately 50% of patients. A genetic predisposition is linked to HLA-DR4.


Etiology
The exact cause is unknown. Genetic, environmental, and autoimmune factors are believed to contribute.


Diagnosis
The diagnosis is supported by the presence of three or more of the following in a patient with vasculitis: age greater than 50 years, erythrocyte sedimentation rate greater than 50 mm/hr, new-onset localized headache, temporal artery tenderness or decreased pulsation, new visual symptoms, and biopsy demonstrating necrotizing arteritis.


Signs And Symptoms
Symptoms may be acute, subacute, or chronic. Headache is the most common symptom, occurring in approximately 70% of patients, and is often unilateral, localized to the temple, and described as boring or lancinating. Jaw or tongue claudication with chewing occurs in about 50%. Constitutional symptoms include fatigue, malaise, anorexia, weight loss, weakness, arthralgias, and low-grade fever.
Visual manifestations usually involve one eye and may develop weeks to months after other symptoms. These include amaurosis fugax, blindness, diplopia, ptosis, extraocular muscle weakness, scotomata, and blurred vision. Visual impairment typically does not improve, even with treatment.
Other findings include scalp tenderness, especially over the temporal artery; early increased pulsations followed by decreased pulsations later in disease; erythema, warmth, swelling, or nodules over scalp arteries; bruits or diminished pulses over large arteries; sore throat, cough, and dysphagia. Neurologic manifestations such as neuropathies, transient ischemic attacks, and strokes may occur in up to one-third of patients. Occult manifestations include glossitis, lingual infarction, tongue infarction, and Raynaud phenomenon. Up to 30% of patients may lack classic symptoms.
Polymyalgia rheumatica is frequently associated, characterized by morning stiffness and aching pain of proximal muscles that improves with activity and may be accompanied by synovitis, particularly in the knees.


Essential Workup
A focused physical examination should emphasize the temporal arteries and scalp, a complete neurologic examination, and a detailed ophthalmic examination including visual acuity and visual fields. Fundoscopy may be normal early but can show optic nerve edema, pallor, hemorrhages, cotton-wool spots, and exudates later. Pulse asymmetry or bruits over large arteries should be documented.


Diagnosis Tests And Interpretation
Laboratory findings typically include a markedly elevated ESR, often greater than 100 mm/hr, and elevated C-reactive protein. Mild normochromic anemia and mild thrombocytosis are common. White blood cell count is usually normal or mildly elevated. Liver enzymes and prothrombin time may be elevated, while renal function and urinalysis are usually normal. Interleukin-6 levels are elevated during disease flares.
Imaging may include Doppler ultrasound showing decreased flow and a characteristic halo sign in temporal arteries. MRI can assess large-vessel involvement. Angiography may reveal smooth, tapered stenoses or occlusions.
Temporal artery biopsy is the diagnostic gold standard and should include multiple sections. It should be performed as soon as feasible after starting steroids. If the initial biopsy is negative and suspicion remains high, contralateral biopsy is recommended.


Differential Diagnosis
Other vasculitides including polyarteritis nodosa, hypersensitivity vasculitis, systemic lupus erythematosus, Takayasu arteritis, and granulomatosis with polyangiitis; retinal, ophthalmic, or temporal artery thrombosis; Lyme disease; and nonarteritic anterior ischemic optic neuropathy.


Treatment Prehospital
Symptoms may be mistaken for stroke. Provide monitoring and supplemental oxygen. Hypotension may occur from rare complications such as aortic dissection, abdominal aortic aneurysm, or myocardial infarction.


Initial Stabilization Therapy
Although uncommon, patients may present with vascular catastrophes requiring aggressive early management consistent with standard emergency protocols.


Ed Treatment Procedures
High-dose corticosteroids are the cornerstone of therapy. When clinical suspicion is strong, steroid treatment should not be delayed for biopsy, as vascular pathologic changes persist for weeks. Early aggressive treatment significantly reduces the risk of blindness. Systemic and local symptoms typically improve within days to weeks, but treatment may be required for several years, with an average disease course of three to four years. Analgesia with NSAIDs, salicylates, or narcotics may be provided as needed.


Medication
Prednisone 60–100 mg orally daily for at least two weeks before tapering. For acute visual symptoms, intravenous methylprednisolone 1,000 mg daily for one to three days may be used. Low-dose aspirin is recommended to reduce thrombotic risk. NSAIDs or narcotics may be used for pain control.


Follow-Up Disposition
Admission is indicated for patients with acute visual loss, impending vascular complications, or acute focal neurologic deficits. Less symptomatic patients without evidence of end-organ damage may be discharged with close follow-up arranged within one to two days.


Issues For Referral
Rheumatology for disease management, ophthalmology for visual symptoms, and neurology for focal neurologic findings.


Follow-Up Recommendations
Ongoing care with rheumatology for steroid management and evaluation for associated connective tissue disease. Ophthalmology and neurology follow-up are required for visual or neurologic involvement.


Key Clinical Insights And Common Errors
Permanent visual loss is the most feared complication. Steroid therapy must not be delayed when clinical suspicion is high or visual symptoms are present. Jaw claudication and amaurosis fugax are often underreported and should be specifically queried. Between 25% and 50% of patients with untreated unilateral visual loss will progress to bilateral blindness.

Emergency And Acute Medicine - GHB Poisoning


Basics Description
γ-Hydroxybutyrate (GHB) is a naturally occurring analog of γ-aminobutyric acid (GABA). It has limited medical use, most notably in narcolepsy. Nonmedical use includes bodybuilding, recreational euphoria, and use as a predatory or date-rape drug. Precursors such as γ-butyrolactone (GBL), 1,4-butanediol (1,4-BD), γ-hydroxyvalerate (GHV), and γ-valerolactone (GVL) produce similar clinical effects. Onset typically occurs 15–30 minutes after ingestion, with duration of effects lasting approximately 2–6 hours.


Etiology
GHB toxicity results from deliberate or accidental ingestion of GHB or its precursors.


Diagnosis Signs And Symptoms
Central nervous system findings include CNS depression, dizziness, ataxia, impaired judgment, aggressive behavior, clonic extremity movements, coma, and seizures. Pulmonary manifestations include respiratory depression, apnea, and rarely laryngospasm. Gastrointestinal symptoms include nausea and vomiting. Cardiovascular effects include bradycardia, atrioventricular block, and hypotension. Other findings include nystagmus and hypothermia.
Withdrawal may present with hypertension, tachycardia, hyperthermia, agitation, diaphoresis, tremors, nausea, vomiting, abdominal cramping, hallucinations, delusions, and psychosis.


Essential Workup
Diagnosis is primarily clinical and based on history and presentation. Coingestants should be excluded if the clinical picture is atypical for GHB intoxication.


Diagnosis Tests And Interpretation
Confirmatory GHB testing is usually a send-out laboratory test and does not affect emergency department management. Urine toxicology screening may help identify coingestants. Serum ethanol level should be obtained. Urinalysis and creatine kinase are indicated if rhabdomyolysis is suspected. ECG may demonstrate sinus bradycardia or atrioventricular block. Chest radiography is indicated if aspiration pneumonia is suspected. Head CT should be considered if occult head trauma is possible.


Differential Diagnosis
Alcohol intoxication, barbiturate overdose, benzodiazepine overdose, neuroleptic overdose, opiate overdose, alcohol withdrawal, and sedative–hypnotic withdrawal.


Treatment Prehospital
All pills, containers, and drug paraphernalia involved in the overdose should be transported with the patient for identification.


Initial Stabilization Therapy
Airway management is the priority. Supplemental oxygen should be administered, and intubation performed if indicated. In patients with depressed mental status, administer thiamine, check glucose with bedside testing, provide dextrose if needed, and administer naloxone.


Ed Treatment Procedures
Management is primarily supportive. Bradycardia may be treated with atropine or temporary pacing. Hypotension is managed with intravenous 0.9% normal saline boluses, Trendelenburg positioning, and dopamine infusion if needed. Seizures should be treated initially with benzodiazepines; refractory seizures may require phenobarbital. Withdrawal should be treated aggressively with benzodiazepines, with phenobarbital or propofol used if benzodiazepines are insufficient.


Medication
Dextrose 50–100 mL of D50 IV (pediatrics: D25 2 mL/kg). Diazepam 5–10 mg IV. Lorazepam 2–4 mg IV. Dopamine infusion 2–20 μg/kg/min. Naloxone 0.4–2 mg IV or IM. Phenobarbital loading dose 10–20 mg/kg IV. Propofol loading dose 0.5–1 mg/kg IV followed by infusion. Thiamine 100 mg IV or IM.


Follow-Up Disposition
Admission is required for intubated patients, those with hypothermia or hemodynamic instability, or suspected coingestions that prolong intoxication. Discharge may be considered after at least 6 hours of observation if the patient is asymptomatic and shows no signs of withdrawal.
Alert: GHB withdrawal is life-threatening and closely resembles alcohol withdrawal; prolonged inpatient treatment may be necessary.


Follow-Up Recommendations
Patients with recreational drug use should receive substance abuse referral. Accidental poisonings require poison prevention counseling. Intentional ingestions require psychiatric evaluation.


Key Clinical Insights And Common Errors
Persistent altered mental status should prompt evaluation for non-toxicologic causes. Routine hospital toxicology screens do not reliably detect GHB or many recreational drugs of abuse.

Emergency And Acute Medicine - Geriatric Trauma


Overview And Scope
Geriatric trauma addresses the unique challenges involved in the evaluation and management of injured older adults. Management should follow standard trauma principles while incorporating age-related physiologic changes, comorbid illnesses, and medication effects. Advanced age, commonly defined as over 65 years, is an independent risk factor for poor outcomes after trauma. Chronologic age does not always reflect physiologic reserve, requiring individualized assessment.


Epidemiology And Risk Profile
Trauma-related morbidity and mortality rise significantly with increasing age. Older adults experience higher complication rates, longer hospitalizations, and increased mortality compared with younger patients sustaining similar injuries. Even low-energy mechanisms can result in severe injury because of diminished physiologic reserve.


Common Mechanisms Of Injury
Falls are the leading cause of injury in patients older than 65 years and frequently occur from standing height or flat surfaces. Motor vehicle collisions are the second most common cause and the leading fatal mechanism. Pedestrian–vehicle collisions occur more often due to impaired vision, hearing, gait, and cognition. Burns carry higher fatality rates compared with younger adults for similar burn size. Violence is less common but should raise concern for elder abuse, which is often underrecognized. Elderly patients are particularly vulnerable to serious injury from low-energy trauma.


Triage And Initial Assessment
Thresholds for trauma activation and transfer to major trauma centers should be lower in elderly patients. Any injured older adult with potential need for surgical, neurosurgical, or orthopedic intervention should be considered for trauma center care.


Clinical Evaluation And Survey Approach
Assessment follows the same primary and secondary survey structure used for all trauma patients, but normal vital signs may be misleading. Hypoperfusion is often masked by blunted physiologic responses, chronic disease, and medication effects.


Airway And Cervical Spine Considerations
Airway management may be more difficult due to dentures, cervical arthritis, temporomandibular joint disease, and limited neck mobility. Early intubation should be strongly considered, as delayed airway control is a common and dangerous error.


Breathing And Ventilation Assessment
Age-related changes in chest wall compliance and weakened respiratory muscles reduce ventilatory reserve. Blunted responses to hypoxia and hypercapnia delay clinical deterioration. A lower threshold for intubation is recommended, and adequate analgesia for chest wall pain is essential to maintain ventilation.


Circulatory And Hemodynamic Evaluation
Heart rate and blood pressure may not accurately reflect cardiac output or shock severity. Chronotropic response to hypovolemia is often impaired, and medications such as beta-blockers and calcium channel blockers blunt tachycardia. Baseline hypertension may conceal relative hypotension. Antiplatelet and anticoagulant therapy increases bleeding risk.


Neurologic Status And Disability Assessment
Rapid neurologic evaluation is critical. Cerebral atrophy may delay the presentation of intracranial hemorrhage, and mental status changes should never be attributed solely to dementia or baseline cognitive impairment. Anticoagulated patients are at increased risk for delayed intracranial bleeding.


Exposure And Secondary Survey
Complete exposure is necessary to identify injuries, while actively preventing hypothermia. After stabilization, a thorough head-to-toe examination and complete secondary survey should be performed.


History And Comorbid Conditions
Elderly trauma patients must be evaluated as both trauma and medical patients. Comorbidities, medications, and allergies are central to management. Medical events such as syncope, hypoglycemia, arrhythmia, stroke, or infection may precipitate trauma. Details of the mechanism and prehospital care should be obtained from emergency medical services whenever possible.


Diagnostic Testing And Imaging Strategy
Baseline studies include CBC, arterial blood gas, electrolytes, renal function, glucose, coagulation profile, lactate, base deficit, and blood typing. Cervical spine and chest imaging are mandatory in major trauma. Liberal use of head CT is recommended for elderly patients with head injury. CT imaging is often preferred over plain radiographs due to degenerative changes. Abdominal trauma evaluation depends on hemodynamic stability, with CT using IV contrast for stable patients and FAST or diagnostic peritoneal lavage for unstable patients. Renal function should be assessed prior to contrast administration.


Prehospital Management Priorities
Key priorities include airway control, hemorrhage management, immobilization, shock treatment, and rapid transport to an appropriate trauma facility.


Initial Resuscitation And Stabilization
Airway management must account for anatomic challenges. Supplemental oxygen, continuous pulse oximetry, capnography, and serial blood gases help monitor respiratory reserve. Circulatory resuscitation should use cautious crystalloid boluses of 250–500 mL with early consideration of red blood cell transfusion. Over-resuscitation can precipitate heart failure. Serial lactate and base deficit measurements guide shock management. Renal perfusion must be protected due to reduced creatinine clearance.


Injury Patterns Common In The Elderly
Head injuries more commonly result in subdural rather than epidural hematomas. Cervical spine injuries, particularly C1–C2 and odontoid fractures, often occur after minor trauma. Vertebral compression fractures are frequent. Rib fractures significantly increase pneumonia risk and mortality with each additional fracture. Abdominal injury patterns are similar to younger adults but require high clinical suspicion. Pelvic and hip fractures are common due to osteoporosis and require early definitive management to restore mobility.


Emergency Department Management Principles
Early cardiopulmonary monitoring, prompt stabilization, and rapid surgical consultation are essential. Definitive management is often surgical. Elderly patients benefit from aggressive yet carefully balanced trauma care, ideally within trauma centers. Advance directives and goals of care should be identified as early as possible.


Disposition And Admission Decisions
Most elderly patients with significant trauma should be admitted for observation or intensive monitoring. A lower threshold for ICU admission is appropriate for polytrauma, chest wall injuries, abnormal vital signs, or evidence of hypoperfusion. Patients with minor trauma and negative evaluations may be observed and discharged if stable.


Follow-Up And Referral Planning
Follow-up and specialty referral depend on the injuries sustained and must be clearly arranged prior to discharge.


Clinical Insights And Common Errors
Seemingly minor mechanisms can cause serious injury due to limited physiologic reserve. Medications such as beta-blockers and anticoagulants complicate assessment and management. Normal blood pressure and heart rate do not exclude shock. Geriatric trauma patients must always be managed as both trauma and medical patients.

Emergency And Acute Medicine - Gastrointestinal Bleeding


Basic Overview
Gastrointestinal bleeding refers to blood loss originating anywhere along the GI tract. Upper gastrointestinal bleeding arises proximal to the ligament of Treitz, whereas lower gastrointestinal bleeding occurs distal to the ligament of Treitz to the anus. Overall mortality is approximately 10%, ranging from less than 5% in children to as high as 25% in adults older than 70 years. Upper GI bleeding accounts for most cases, with nonvariceal mortality of 6–8% and variceal bleeding mortality of 30–50%. Lower GI bleeding carries a mortality of 2–4%.


Common Causes And Mechanisms
Upper GI bleeding is most frequently due to ulcerative disease, particularly peptic ulcer disease associated with Helicobacter pylori infection or medication use such as NSAIDs, aspirin, glucocorticoids, potassium, and iron supplements. Other causes include gastric or esophageal erosions, reflux esophagitis, infectious esophagitis, pill-induced injury, foreign bodies, gastritis, and stress-related mucosal disease from trauma, burns, sepsis, or CNS injury. Portal hypertension leads to esophageal or gastric varices and portal hypertensive gastropathy. Vascular causes include arteriovenous malformations, Dieulafoy lesions, gastric antral vascular ectasia, and aortoenteric fistulas. Mallory–Weiss tears, tumors, pancreatic hemorrhage, hemobilia, and parasitic infections are less common causes.
Lower GI bleeding most often results from diverticulosis, colorectal cancer or polyps, colitis (ischemic, inflammatory, infectious, or radiation-induced), angiodysplasia, postpolypectomy bleeding, inflammatory bowel disease, anorectal sources such as hemorrhoids or fissures, rectal ulcers, and foreign bodies. In children, Meckel diverticulum and intussusception are the leading causes.


Clinical Presentation
Both upper and lower GI bleeding may present with hypovolemia. Upper GI bleeding typically causes hematemesis or coffee-ground emesis and melena, whereas lower GI bleeding usually presents with hematochezia. Rapid upper GI bleeding can also cause hematochezia. Patients may report abdominal pain, weakness, dizziness, dyspnea, confusion, or agitation.


History And Physical Examination
Key historical features include vomiting blood, black or tarry stools, bright red blood per rectum, abdominal pain, and symptoms of anemia or shock. Examination may reveal tachycardia, hypotension, pallor, dry mucous membranes, melena or hematochezia on rectal exam, and signs of shock.


Initial Evaluation Priorities
Essential evaluation includes CBC, coagulation studies, electrolytes, and assessment for hypovolemia. ENT examination helps differentiate hematemesis from hemoptysis. Nasogastric lavage may assist in identifying active upper GI bleeding, though its impact on outcomes is controversial. Rectal examination is necessary to assess stool color and identify anorectal sources while recognizing causes of false-positive or false-negative fecal occult blood tests.


Diagnostic Testing
Laboratory studies may reveal anemia, thrombocytopenia, coagulopathy, electrolyte abnormalities, elevated BUN-to-creatinine ratio suggestive of upper GI bleeding, and elevated lactate in shock. Imaging may include upright chest radiography if perforation or aspiration is suspected. Angiography and radionuclide scans can localize active bleeding. Endoscopic evaluation with esophagogastroduodenoscopy is diagnostic and therapeutic for upper GI bleeding, while colonoscopy is primarily diagnostic for lower GI bleeding after bowel preparation.


Differential Diagnosis
Alternative sources of apparent GI bleeding include epistaxis, oropharyngeal bleeding, hemoptysis, hematuria, vaginal bleeding, and traumatic injuries.


Prehospital Management
Airway protection is critical in massive bleeding or altered mental status. Large-bore IV access should be established, and crystalloid infusion initiated to maintain systolic blood pressure above 90 mm Hg.


Emergency Department Stabilization
Airway, breathing, and circulation are prioritized. Two large-bore IV lines are placed, cardiac monitoring initiated, and volume resuscitation started with crystalloid boluses. Blood transfusion is indicated for significant anemia or hemodynamic instability, with attention to balanced transfusion strategies in massive hemorrhage. Coagulopathy is corrected with fresh frozen plasma, vitamin K, and platelets as indicated.


Definitive Emergency Treatment
Early gastroenterology consultation is essential. Proton pump inhibitor infusion is initiated for suspected upper GI bleeding, and octreotide is added when variceal bleeding is suspected. Vasopressin may be considered for refractory variceal bleeding with caution. Emergent endoscopy provides definitive diagnosis and therapy, including cauterization, injection, or banding. Balloon tamponade is reserved as a last resort. In cirrhotic patients, prophylactic antibiotics reduce mortality. For lower GI bleeding, angiography or surgical intervention may be required for ongoing massive hemorrhage.


Medication Therapy
Management includes IV proton pump inhibitors, octreotide or somatostatin analogs, vasopressors when indicated, nitroglycerin with vasopressin to limit ischemia, and vitamin K for coagulopathy.


Disposition And Admission Criteria
Admission is required for active bleeding, advanced age, comorbid illness, coagulopathy, anemia, or any episode of hemodynamic instability. Discharge may be considered for resolved bleeding with negative evaluation, stable hematocrit, and reliable follow-up in otherwise healthy patients.


Follow-Up And Referral
Patients discharged from the emergency department require close follow-up within 24–36 hours and clear return precautions. Upper GI bleeding patients should continue proton pump inhibitor therapy and avoid alcohol, NSAIDs, aspirin, caffeine, and tobacco.


Key Clinical Pearls And Pitfalls
A significant proportion of upper GI bleeding presents with hematochezia. Failure to aggressively resuscitate with fluids and blood products is a common and dangerous error. In elderly patients, peptic ulcer disease remains the most common cause and is associated with higher mortality.

Emergency And Acute Medicine – Head Pain Syndromes


Overview And Pathophysiology
Headache is pain perceived in the cranium, orbits, or upper cervical region. Pain originating from intracranial structures is often projected to the surface. Intracranial pain-sensitive structures include arteries, veins, dura, and meninges. Extracranial sources include the skin, scalp, fascia, muscles, mucosal linings of the sinuses, arteries, temporomandibular joints, and teeth. Pain transmission occurs primarily via the trigeminal (V) cranial nerve. Mechanisms include nerve irritation, traction on pain-sensitive vessels, vasodilation, hypoxia, hypercapnia, fever, histamine exposure, or nitroglycerin ingestion. Headache accounts for 2–4% of ED visits; approximately 95% are benign, though serious etiologies are more common in patients older than 50 years.


Causes And Risk Factors
Migraine results from intra- and extracranial vasodilation and constriction of pain-sensitive vessels and may involve cortical spreading depression. Pain is typically throbbing. Tension-type headache requires at least ten similar episodes and has an unclear etiology, possibly involving serotonin imbalance, reduced endorphins, or muscle spasm. It is the most common recurrent headache, often triggered by poor posture, stress, anxiety, depression, or cervical osteoarthritis. Pain is usually bilateral, nonpulsatile, band-like, mild to moderate, and lasts 4–13 hours.
Cluster headache may be triggered by alcohol, certain foods, sleep disruption, or strong emotions and may involve vasospasm near cranial nerves.
Intracranial pressure or traction causes include mass lesions and idiopathic intracranial hypertension. Extracranial compression headaches arise from peripheral nerve pathology of the head and neck. Inflammatory causes include temporal arteritis and cerebral vasculitis. Thrombotic causes include cerebral venous sinus thrombosis. Disorders of vascular autoregulation include posterior reversible leukoencephalopathy syndrome and reversible cerebral vasoconstriction syndrome.
Children rarely have serious headache causes but require follow-up. Older adults with new-onset headache have higher risk for serious disease and warrant low thresholds for imaging. Pregnancy and the postpartum period increase risk for CVST, eclampsia, PRES, and RCVS.


Clinical Assessment
History should characterize pain using PQRST. Provoking factors include head position, coughing, or straining; worsening with these suggests elevated intracranial pressure. Quality may be throbbing or continuous, deep or superficial. Assess region, severity, “worst headache of life,” timing (sudden vs. gradual), and associated symptoms such as visual changes, dizziness, nausea, or vomiting.
Red flags include new onset, age >50 years, immunosuppression, malignancy, trauma or falls, persistent vomiting, focal neurologic or visual deficits, and risk factors for CVST (pregnancy/postpartum, malignancy, oral contraceptives, protein C/S deficiency, ulcerative colitis, Behçet syndrome).


Physical Examination
Perform a complete neurologic exam including cranial nerves, motor and sensory testing, reflexes, and gait. Examine fundi for papilledema. Inspect skin for rashes (e.g., zoster, purpura). Palpate temporal arteries for tenderness or thickening.


Initial Evaluation Strategy
A thorough history and focused CNS, HEENT, and neck examination are essential. Additional testing is indicated with severe hypertension, fever, altered mental status, papilledema, abnormal neurologic findings, or meningismus.


Diagnostic Studies
Laboratory testing includes cerebrospinal fluid analysis when meningitis or subarachnoid hemorrhage is suspected and ESR when temporal arteritis or inflammatory disease is considered.
Noncontrast head CT is indicated for uncertain diagnosis, signs of increased ICP, first or worst headache, abrupt onset, new focal deficits, papilledema, recurrent morning headaches, persistent vomiting, headache with fever or rash, trauma with LOC, altered mental status, or meningismus. CT within 6 hours of onset is highly sensitive for SAH; sensitivity declines after 24 hours.
MRI evaluates posterior fossa lesions, pituitary apoplexy, CVST, and causes missed by CT and LP. MRA is indicated when SAH is suspected with negative CT and LP cannot be performed, or when arterial dissection or nonmigrainous vascular causes are suspected.
Lumbar puncture is required after CT when focal deficits, papilledema, abnormal mental status, or immunosuppression are present. It detects infection, occult SAH, opening pressure abnormalities, and distinguishes traumatic tap from hemorrhage. Xanthochromia is typically present by 12 hours after SAH onset.


Differential Diagnosis
Acute single headache includes SAH, meningitis, intracerebral hemorrhage, hypertensive encephalopathy, arterial dissection, CVST, cerebellar stroke, acute angle-closure glaucoma, pituitary apoplexy, temporal neuritis, trauma, acute sinusitis, toxic or metabolic states, withdrawal syndromes, and post–lumbar puncture headache.
Acute recurrent headache over days to weeks includes migraine, cluster, tension, CVST, pseudotumor cerebri, temporal arteritis, SAH rebleed, hypoxia-related headache, trigeminal neuralgia, postherpetic neuralgia, exertional and coital headaches.
Subacute headache over weeks to months suggests chronic subdural hematoma, brain tumor, brain abscess, chronic sinusitis, temporomandibular joint disorders, chronic post-traumatic headache, pseudotumor cerebri, or temporal arteritis.
Chronic headache over months to years includes chronic tension headache, medication overuse headache, depression-related headache, trigeminal neuralgia, severe anemia, acute glaucoma, and cervical spine disease.


Management Principles
Initial stabilization focuses on airway, breathing, and circulation in patients with altered mental status. Start empiric antibiotics promptly for suspected bacterial meningitis and add acyclovir in immunocompromised patients.
ED management is etiology-specific. Migraine, cluster, and tension headaches receive symptomatic therapy. Temporal arteritis, intracranial infection, and intracranial hemorrhage require targeted treatment.


Disposition And Follow-Up
Admit patients with suspected organic disease, intractable vomiting with dehydration, or pain refractory to outpatient therapy. Consider ICU admission for suspected aneurysm, acute subdural hematoma, SAH, stroke, increased ICP, or intracranial infection.
Discharge is appropriate for resolved migraine, cluster, or tension headaches and minor infections with adequate follow-up. Patients with recurrent headaches should follow up with a primary care physician or neurologist.


Medications Commonly Used
Common agents include chlorpromazine, dexamethasone, dihydroergotamine, ergotamine, ketorolac, intranasal lidocaine, metoclopramide, morphine, prochlorperazine, and sumatriptan, selected based on headache type and patient factors.


Clinical Warnings And Pitfalls
Do not use treatment response to determine benign etiology. CT sensitivity for SAH decreases rapidly after 24 hours; lumbar puncture remains essential after delayed presentation. Neurology consultation should not delay urgent imaging in high-risk cases. Use dopamine antagonists cautiously in QT prolongation or electrolyte abnormalities. Use triptans and ergotamines cautiously in coronary artery disease. Chronic headache patients benefit from consistent plans, but new or changing features require reassessment. Never delay empiric treatment of suspected meningitis while awaiting lumbar puncture results.

Emergency And Acute Medicine - Gastroesophageal Reflux Disease


Basic Overview
Gastroesophageal reflux disease represents a spectrum of conditions in which reflux of gastric contents produces symptoms and mucosal injury of the esophagus. This includes erosive reflux esophagitis and nonerosive reflux disease. Up to 40% of the general population experience reflux symptoms at least monthly.


Pathophysiology And Predisposing Factors
GERD results from failure of the antireflux barrier, allowing increased frequency and duration of gastric acid exposure to the esophagus. The lower esophageal sphincter is the primary barrier, with additional contribution from the crural diaphragm at the gastroesophageal junction. Esophageal acid clearance through peristalsis and intrinsic mucosal resistance further protect against injury. Transient lower esophageal sphincter relaxations occur more frequently in GERD and are a major mechanism of reflux. Repeated acid exposure leads to mucosal acidification, inflammation, necrosis, and complications over time. Reduced LES tone is associated with smoking, alcohol, chocolate, coffee, tea, onions, and medications such as calcium channel blockers, nitrates, opioids, barbiturates, and theophylline. Delayed gastric emptying, obesity, gastric distention, and increased intra-abdominal pressure also contribute. Hiatal hernias may be associated but are not uniformly symptomatic. Associated conditions include pregnancy, diabetes mellitus, hypothyroidism, neurologic disorders, and autoimmune disease.


Clinical Manifestations
Esophageal symptoms include heartburn, regurgitation, and dysphagia. Extraesophageal manifestations include chronic cough, bronchospasm, laryngitis, hoarseness, and recurrent pneumonitis. Patients commonly describe retrosternal burning pain radiating from the epigastrium to the neck, often worse when supine or bending forward and temporarily relieved by antacids. Dysphagia suggests esophageal spasm or stricture, while odynophagia raises concern for ulcerative esophagitis. Atypical presentations include noncardiac chest pain, asthma exacerbations, hiccups, throat clearing, nocturnal choking, and upper gastrointestinal bleeding.


Physical Examination Findings
Physical examination is often nonspecific and may reveal mild epigastric tenderness. Symptoms may worsen when the patient is placed supine or in the Trendelenburg position.


Special Considerations In Children
Physiologic reflux is common in infants and typically resolves with age. Concerning features include persistent vomiting, irritability, feeding refusal, failure to thrive, arching during feeds, and respiratory symptoms.


Initial Assessment Priorities
The primary goal is to exclude emergent conditions such as acute coronary syndrome, esophageal perforation, or aortic pathology. A focused history and complete physical examination, including vital signs and cardiopulmonary evaluation, are essential.


Diagnostic Evaluation
There is no single gold standard diagnostic test. Laboratory studies may show chronic anemia from esophagitis or occult bleeding. Routine imaging is not required, though chest radiography may identify perforation, hiatal hernia, or aortic disease when suspected. A therapeutic trial of acid suppression is often diagnostic, with approximately 90% of patients responding to proton pump inhibitor therapy. Further testing is reserved for refractory or complicated cases and includes barium esophagram for dysphagia, esophageal pH monitoring to correlate symptoms with acid exposure, manometry to assess motility, and upper endoscopy to evaluate for esophagitis, Barrett esophagus, strictures, ulcers, or malignancy.


Differential Diagnosis
Conditions that may mimic GERD include ischemic heart disease, asthma, peptic ulcer disease, gastritis, pancreatitis, hepatitis, esophageal infection or perforation, biliary disease, and mesenteric ischemia.


Prehospital Considerations
Esophageal pain may resemble angina, and airway protection may be required in patients with significant vomiting.


Stabilization And Early Management
Assessment of airway, breathing, and circulation is required. IV fluids are administered for bleeding or shock.


Emergency Department Management
Initial therapy focuses on symptom relief and acid suppression. Antacids, antacids combined with viscous lidocaine, and sublingual nitroglycerin may relieve esophageal spasm. Lifestyle modification is a cornerstone of therapy and includes avoidance of late or heavy meals, remaining upright after eating, head-of-bed elevation, weight reduction, smoking and alcohol cessation, and avoidance of foods and medications that reduce LES tone. Proton pump inhibitors are the most effective agents for healing esophagitis and controlling moderate to severe disease. H2-receptor antagonists are effective for mild to moderate symptoms. Adjunctive agents include alginic acid, sucralfate, and prokinetic agents such as metoclopramide. Endoscopic therapies and antireflux surgery, including fundoplication or incisionless techniques, are reserved for selected patients with refractory disease or complications.


Pregnancy-Specific Considerations
GERD is common during pregnancy due to hormonal changes and increased intra-abdominal pressure. H2 blockers are first-line therapy because of their safety profile, while PPIs are used cautiously. Endoscopy is reserved for severe or complicated cases.


Medication Options
Therapy includes antacids, H2 blockers, proton pump inhibitors, sucralfate, and prokinetic agents. Choice depends on disease severity, comorbidities, and patient-specific factors.


Disposition And Follow-Up
Hospital admission is indicated for significant esophageal bleeding, uncontrolled asthma related to reflux, dehydration, or failure to thrive. Patients with uncomplicated disease may be discharged with outpatient follow-up through primary care or gastroenterology.


Referral And Long-Term Care
Gastroenterology referral is recommended for patients with persistent symptoms requiring long-term therapy, alarm features, or suspected complications such as Barrett esophagus.


Key Clinical Insights And Pitfalls
Effective management of GERD requires both lifestyle modification and pharmacologic therapy. Proton pump inhibitors are preferred for moderate to severe disease or erosive esophagitis. Failure to respond to therapy warrants endoscopic evaluation. Surgical intervention may benefit selected young patients requiring lifelong high-dose acid suppression. Common complications include esophagitis, peptic stricture, Barrett metaplasia, and extraesophageal manifestations such as asthma and chronic cough.

Emergency And Acute Medicine - Gastroenteritis


Basic Overview
Gastroenteritis is an inflammatory condition of the stomach and intestines characterized by diarrhea and vomiting, most commonly caused by infectious agents or exposure to toxins.


Causes And Risk Factors
Infectious causes account for most cases. Viruses are responsible for approximately 50–70% of cases, with norovirus increasingly common among travelers, particularly those returning from Mexico and India. Invasive bacterial causes include Campylobacter, the most common bacterial pathogen, typically acquired from contaminated food, water, or animal exposure and often associated with gross or occult blood in stool. Salmonella is linked to contaminated water, eggs, poultry, or dairy products, with Salmonella typhi causing typhoid fever characterized by persistent fever, abdominal pain, rose spots, splenomegaly, and relative bradycardia. Shigella spreads via the fecal–oral route, while Vibrio parahaemolyticus is associated with raw or undercooked seafood. Yersinia infections arise from contaminated pork, water, or milk and may mimic appendicitis due to mesenteric adenitis. Food-borne toxin-mediated illnesses include Staphylococcus aureus, with symptoms appearing within 1–6 hours, and Bacillus cereus, classically associated with reheated rice, with symptoms developing within 1–36 hours. Cholera causes profuse watery diarrhea described as rice-water stools. Ciguatera poisoning follows fish ingestion and presents with neurologic symptoms such as paresthesias and hypotension. Scombroid poisoning results from spoiled fish and causes flushing, headache, and burning sensations, usually resolving within hours. Protozoal causes include Giardia lamblia, particularly in travelers, campers drinking untreated water, daycare children, and men who have sex with men. Noninfectious causes include heavy metals, organic chemicals, pesticides, radioactive substances, and adverse reactions to food additives. In pediatric patients, most cases are viral and self-limited, with rotavirus being common; Shigella infections may be associated with seizures.


Clinical Features And Presentation
Patients commonly present with nausea, vomiting, diarrhea, abdominal cramps, fever, malaise, myalgias, headache, and anorexia. Bloody or mucous stools suggest invasive disease. Severe cases may involve hypotension, lethargy, and dehydration.


Physical Examination Findings
Findings may include dry mucous membranes, tachycardia, abdominal tenderness, and perianal irritation such as fissures or fistulas, reflecting dehydration or inflammatory diarrhea.


Initial Evaluation And Assessment
Evaluation should include a digital rectal examination to assess for gross or occult blood. Stool leukocyte testing may help differentiate invasive bacterial infections, where leukocytes are present, from viral, protozoal, or toxin-mediated illnesses.


Laboratory And Imaging Evaluation
CBC is indicated in cases of significant blood loss or systemic toxicity. Electrolytes, glucose, BUN, and creatinine should be obtained in patients with lethargy, dehydration, toxicity, altered mental status, or underlying renal or liver disease. Stool cultures are indicated when fecal leukocytes are present, in immunocompromised patients, travelers, food handlers, and healthcare or daycare workers. Blood cultures are reserved for suspected bacteremia, severe systemic illness, or high-risk populations such as the elderly, infants, and immunocompromised patients. Imaging has limited value and is reserved for suspected obstruction or toxic megacolon. In children, laboratory testing is usually unnecessary unless toxicity or immunocompromise is present.


Differential Diagnosis Considerations
Conditions to consider include gastritis, peptic ulcer disease, food allergies, appendicitis, irritable bowel syndrome, inflammatory bowel disease, malrotation with volvulus, Meckel diverticulum, medication-induced diarrhea, and toxin exposures.


Prehospital Management
Establish IV access in patients with severe dehydration and minimize exposure to contaminated body fluids or clothing.


Stabilization And Early Treatment
Management focuses on airway, breathing, and circulation. Severely dehydrated patients require IV fluid resuscitation with 0.9% normal saline.


Emergency Department Care
Oral rehydration with electrolyte solutions is appropriate for mild dehydration. IV fluids are indicated for hypotension, persistent vomiting, altered mental status, metabolic derangements, or severe dehydration, using weight-appropriate boluses followed by maintenance fluids. Bismuth subsalicylate provides symptomatic relief and has antisecretory effects. Antimotility agents may be used cautiously in noninfectious diarrhea but should be avoided or limited in infectious cases due to the risk of prolonged illness or toxic megacolon. Antibiotics are reserved for specific pathogens such as Campylobacter, Salmonella, Shigella, Vibrio, Clostridium difficile, Escherichia coli, and Giardia. Antiemetics such as ondansetron, prochlorperazine, or promethazine may be used for symptom control.


Medication Options
Treatment may include antibiotics tailored to the identified pathogen, antiemetics, and supportive medications for hydration and symptom relief. Drug selection should consider age, pregnancy status, and comorbid conditions.


Disposition And Follow-Up
Admission is required for patients with refractory hypotension, significant bleeding, sepsis, intractable symptoms, severe electrolyte disturbances, metabolic acidosis, altered mental status, or severe dehydration, particularly in children. Patients with mild disease or dehydration responsive to fluids may be discharged.


Follow-Up Guidance
Most cases are self-limited and do not require routine follow-up. Patients with prolonged or recurrent symptoms may benefit from gastroenterology referral.


Key Clinical Insights And Pitfalls
Viruses cause the majority of gastroenteritis cases. Antimotility agents should be avoided in infectious diarrhea. Several commonly used antibiotics are contraindicated in pregnancy. Early recognition of dehydration and judicious use of antibiotics are critical to optimal management.

Emergency And Acute Medicine - Gastritis


Basics Description
Inflammatory response of the gastric mucosa to injury, referred to as gastritis. The gastric mucosa is protected by three main defense mechanisms: a mucus layer that forms a protective pH gradient, surface epithelial cells capable of repairing small defects, and a postepithelial barrier that neutralizes acid that penetrates the first two layers. There is no definite correlation between histologic gastritis and dyspeptic symptoms. Epithelial cell damage without associated inflammation is termed gastropathy.


Etiology
Common causes of gastritis include infections, autoimmune disease, drugs such as cocaine, hypersensitivity reactions, and physiologic stress. Common causes of gastropathy include endogenous or exogenous irritants such as bile reflux, alcohol, aspirin and other NSAIDs, ischemia, stress, and chronic congestion. Acute gastritis may occur with severe stress states such as sepsis, burns, or trauma due to reduced splanchnic blood flow leading to decreased mucus production, bicarbonate secretion, and prostaglandin synthesis, resulting in mucosal erosions and hemorrhage. Alcohol induces leukotriene production, causing microvascular stasis and increased permeability with hemorrhage. NSAIDs, including aspirin, interfere with prostaglandin synthesis and cause similar mucosal injury. Steroids may also contribute. Chronic gastritis is most commonly caused by Helicobacter pylori, a gram-negative spiral bacterium found in the gastric mucus layer that produces urease, allowing alkalinization of its microenvironment.


Diagnosis Signs And Symptoms
Common symptoms include dyspepsia, bloating, nausea, vomiting, anorexia, epigastric tenderness, and heartburn. History often reveals episodic or chronic epigastric pain or discomfort, indigestion, eructation, flatulence, nausea or vomiting, and in severe cases hematemesis or melena.


Physical Exam Findings
Examination should include careful assessment of vital signs and orthostatics, stool Hemoccult testing, and evaluation for dehydration and tachycardia in patients with vomiting. Pallor may be present in hemorrhagic gastritis. Abdominal examination is often nonspecific but may reveal epigastric tenderness.


Essential Workup
Initial evaluation focuses on airway, breathing, and circulation, with hematocrit determination and assessment for dehydration or shock.


Diagnostic Tests And Interpretation
Laboratory studies are often normal in uncomplicated gastritis. CBC may reveal anemia in acute hemorrhagic gastritis or leukocytosis with infection. Electrolytes, BUN, creatinine, and glucose assess dehydration and metabolic disturbances. Amylase and lipase help exclude pancreatitis. Urinalysis evaluates dehydration or ketosis. Bilirubin may be elevated in hepatitis. ECG is recommended in elderly patients to evaluate for myocardial ischemia. Endoscopy is usually outpatient unless there is significant hemorrhage and allows visualization of bleeding sites, histologic confirmation, and detection of Helicobacter pylori. Noninvasive H. pylori testing includes urea breath tests, stool antigen testing, and serology. Serum pepsinogen isoenzyme ratios may suggest metaplastic atrophic gastritis.


Differential Diagnosis
Peptic ulcer disease, nonulcer dyspepsia, gastroesophageal reflux disease, biliary colic, cholecystitis, pancreatitis, hepatitis, abdominal aortic aneurysm, aortic dissection, and myocardial infarction should be considered.


Treatment Pre Hospital
Initial management includes airway support and intravenous fluid resuscitation as needed.


Initial Stabilization And Therapy
Patients with acute erosive or hemorrhagic gastritis and hemodynamic instability require aggressive fluid resuscitation with lactated Ringer solution or normal saline via two large-bore IV lines. Nasogastric tube placement is indicated for hematemesis or unstable patients, and Foley catheterization may be used to monitor volume status.


Emergency Department Treatment And Procedures
Symptom control includes antacids, gastrointestinal cocktail therapy, H2 receptor antagonists, proton pump inhibitors, and sucralfate. Narcotics should be avoided as they may mask serious illness. Acute hemorrhagic gastritis requires IV fluids, blood transfusion if indicated, and correction of underlying causes such as alcohol use, sepsis, NSAIDs, or trauma. Stress gastritis prevention in critically ill patients involves antacids or IV H2 blockers or proton pump inhibitors to maintain gastric pH above four. Chronic gastritis due to Helicobacter pylori requires eradication therapy with appropriate antibiotic regimens. Vitamin B12 supplementation is indicated in atrophic gastritis.


Medication
Therapeutic options include antacids, H2 blockers, proton pump inhibitors, sucralfate, bismuth subsalicylate, and misoprostol. First-line Helicobacter pylori treatment consists of triple therapy using a proton pump inhibitor with clarithromycin and amoxicillin or metronidazole. Sequential and bismuth-based quadruple therapies are used in high-resistance or treatment-failure settings.


Follow-Up Disposition
Admission is required for patients with acute hemorrhagic or erosive gastritis presenting with upper gastrointestinal bleeding, tachycardia, hypotension, uncontrolled pain or vomiting, or coagulopathy. Stable patients with normal examinations, laboratory results, and heme-negative stools may be discharged. Patients with heme-positive stools may be discharged only if vital signs and hematocrit are stable and nasogastric aspiration is negative.


Follow-Up Recommendations
Close outpatient follow-up with a gastroenterologist is recommended for endoscopy, biopsy, and Helicobacter pylori testing.


Clinical Pearls And Common Errors
Gastritis and gastropathy are common emergency department presentations characterized by dyspepsia, nausea, and vomiting. Management should include both diagnostic evaluation and targeted therapy. Treatment often involves Helicobacter pylori eradication, though antibiotic resistance is increasing. Early gastroenterology follow-up is essential to detect gastric dysplasia or malignancy.