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Abdominal pain approach
- Definition: acute vs. chronic, vital signs.
- History: your patient will give you the answer.
- Physical Exam: location will likely give you Dx (be careful!).
- Imaging: plain films, Ultrasound, CT scans
- Abrupt onset. Consider ECG in epigastric pain with CAD risk factors.
- Dx is based on history and physical examination and laboratory analysis. Early intervention critical.
- Tx may not be surgical. Is the patient Critically Ill? Do the symptoms fit a known dz pattern?
Acute Abdomen Red Flags
Extremes of Age, Severe pain with rapid onset, Abnormal vitals signs, Dehydration, Visceral Involvement
Acute Abdomen Hx
- Peds: Appendicitis, Intussusception, Gastroenteritis, Colic
- Adults: extensive ddx. Bowel habits (change in amount, texture, color, blood), Menstruation (cycle, pain, pregnancy, ectopic), Sexual hx (high risk practices), Drug/Tobacco use.
- Elderly: AAA, Obstruction, Neoplastic Dz.
Acute Abdomen Labs/Imaging
Treat pt, not labs. ABC., CMP, Amylase, Lipase, Lactate, LFTs, UA, stool studies. Plain films, US, CT
Acute Abdomen Consult for
Appendicitis, Cholecystitis, Aortic aneurysm, Bowel obstruction, Ectopic pregnancy, Abscess, Incarcerated hernia, Any acute abdomen without clear dx
Abdominal Visceral Pain
Stretching of unmyelinated fibers in walls or organs. Early ischemia or inflammation. Crampy, dull or achy pain. Patients cannot lie still. Pallor, Diaphoresis or vomiting.
Abdominal Parietal Pain
Irritation of myelinated fibers that innervate the peritoneum. As dz progresses visceral pain gives way to parietal pain. Likely localizes to location of dz. Rigidity and rebound. Immobile patients
Abdominal Referred Pain
Pain at a location distant from the dz organ. Usually perceived on same side as involved organ. Embryological Origins.
Biliary Colic, Cholangitis, Cholecystitis, PUD, MI (atypical), Acute pancreatitis, Herpes zoster, Lower lobe pneumonia, Radiculitis, Congestive hepatomegaly, Hepatitis or hepatitic abscess, Perforated duodenal ulcer, Retrocecal appendicitis (rare)
Gastric Ulcer, Gastritis, Splenic Rupture, Acute pancreatitis, Herpes zoster, Lower lobe pneumonia, Myocardial ischemia, Radiculitis
Aortic Aneurysm, Appendicitis, Crohn’s, Diverticulitis, Ectopic, Endometriosis, Hernia, Colitis, Ovarian cyst, PID, Testicular torsion, Stone, Mesenteric adenitis, Abdominal abscess, Cystitis, Incarcerated/strangulated hernia, Inflammatory bowel dz
Aortic Aneurysm, Sigmoid diverticulitis, Ectopic, Hernia, Colitis, Ovarian cyst, PID, Testicular torsion, Renal Stone, Endometriosis, Abdominal abscess, Cystitis, Incarcerated or strangulated hernia, Inflammatory bowel dz
Diffuse Abdominal Pain
Acute pancreatitis, Mesenteric ischemia, Diabetic ketoacidosis, Peritonitis (any cause), Early appendicitis, Sickle cell crisis, Gastroenteritis, Spontaneous peritonitis, Intestinal obstruction, Typhoid fever. AAA
Acute Abdomen and Vomiting
- Severe irritation of peritoneal or mesenteric nerves.
- Obstruction of an involuntary tube (biliary duct, ureter, intestine, appendix).
- Bilious, bloody or watery.
- Frequency, after meals, morning.
- Pain relief/exacerbation.
- Patient behavior (ridged, colicky, eating)
- Signs of Distention (ascites, ileus, obstruction),
- Obvious Mass (hernia, tumor, aneurysm, knife),
- Scars (post operative scars may indicate chronic dz),
- Liver dz (spider angiomata)
- Decreased Bowel Sounds: ileus, mesenteric infarct, narcotic use, obesity
- Hyperactive Bowel Sounds: (small bowel obstruction (limited), distention
Dull vs Tympanic (fluid vs air), Liver size, Fluid wave (ascities), Always save the painful area for last.
- Voluntary guarding (muscle contraction in anticipation of exam).
- Involuntary guarding (rigid, pain with coughing, bed movement – peritoneal irritation).
- DRE (important part of any abdominal exam).
- Pelvic exam (sexually active female with abdominal pain, do not exclude older female from pelvic exams).
- Testicular exam (hernia, referred pain, sexually active males).
- Hematocrit/Hemoglobin: Low (bleeding, anemia). High (dehydration, COPD).
- WBC High or Low (infection vs cancer). Beware in elderly and very young.
- Differential WBC Increased number of bands (immature WBC).
- Amylase/Lipase Elevated in pancreatitis, small bowel obstruction, salivary gland infection.
- ALT/AST (elevated in hepatitis).
- Bili/Alk Phos (common bile duct obstruction).
- UA Hematuria, UTI, pyelonephritis.
- HCG Assume pregnant until proven otherwise.
- Lactate Mesenteric ischemia, sepsis
Acute Abdomen Imaging
- Plain films (free air evaluations, obstructions).
- Ultrasound (biliary tract dz, renal, ovarian).
- CT scans (includes most abd. dz, consider risks—radiation exposure, contrast material in renal dz; A negative CT does not rule out serious dz )
Acute Abdomen Analgesics
Do not withhold pain medication. Early use of opioid medications does NOT mask an exam or lead to increase morbidities.
Acute Abdomen Antibiotics
Use early if suspected infection or sepsis, target specific gut flora. GI bugs are different than pelvic infections.
Acute Abdomen NSAIDs and Antiemetics
- Caution in NSAID use (ulcer, bleeding disorder, masking inflammation).
- Antiemetics (manage nausea/vomiting, Reglan, Zofran, Phenergan—adverse reactions include sedation, dystonia).
Periumbilical pain radiating to RLQ. Anorexia. Dull pain initially developing into focal, sharp pain. Exam reveals fever, McBurney’s point tenderness. Peak age adolescence and young adults.
Appendicitis Labs, Imaging and Mgt
- Labs (may see WBC elevation, not diagnostic).
- Radiology (CT is preferred in adults and non pregnant women).
- Tx: (surgical Mgt, morbidity increases in perforations)
- Recent surgery or narcotic use. Pain is diffuse, colicky. Will present with nausea/vomiting, distended abdomen.
- Labs (maybe elevated lactate in extreme necrosis).
- Radiology (Plain films~77% sensitive, CT scans~93%).
- Tx: (NPO, NG decompression, IV fluids, Bowel resection)
- Usually M>F <40. LLQ pain. N/V, fever.
- Labs (elevated WBC, 25% + FOBT).
- Imaging (CT 93% sensitive,100% specific).
- Tx (IV fluids, pain Mgt, antiemetics, Antibiotics).
- Complications include abscess, perforation, fistula.
- Severe, sharp, constant R sided abdominal pain, RUQ > epigastric. Can have R shoulder radiating pain. Fever, + Murphy sign, jaundice, N/V. Pain related to meals.
- The 5 F’s (fat, female, flatulent, fertile, 40)
Acute Cholecystitis Workup
- Labs (Elevated WBC, LFT’s, biliary labs).
- Imaging (US, HIDA scan, ERCP).
- Tx (IV fluids, NPO, pain Mgt, Surgical Mgt, Antibiotics in advance cases or perforation)
- Older, male, smoker, underlying cardiovascular dz. Sharp, severe, stabbing mid abdominal pain radiating to back. Occasionally will have pulsatile mass.
- Imaging (Bedside US, CT angiogram for stable aneurysm).
- Tx (Immediate surgical)
- Dx based on risk factors. M>F, ETOH, drug use, biliary dz. Severe upper quadrant, epigastric pain. N/V, fever.
- Labs (↑lipase w/i 24h, ↑ WBC and LFT’s).
- Radiology (CT).
- Tx (IV fluids, pain Mgt, NPO, Bowel rest, Monitor for hemorrhage, sepsis)
- Severe, non focal pain, out of proportion. Fever, N/V. Recent surgical procedure.
- Labs (Elevated lactate in advance cases of ischemia).
- Radiology (Usually not helpful. CT angiogram for vascular occlusion).
- Tx (Surgical vs non operative Mgt)
Ectopic Pregnancy and Acute Salpingitis
- Severe lower abdominal pain, fever, vaginal bleeding,, positive pregnancy test.
- Labs (ABC, T&S, serum HCG).
- Imaging (TVUS).
- Tx (2 large bore IV, NPO, pain control. Surgical vs non operative Mgt. Immediate surgical Mgt vs serial HCGs and ultrasounds)
Deeply unconscious, absent gag reflex. Noninvasive. Prevents blockage of glottis by tongue. Does not prevent aspiration. May cause vomiting, laryngospasm and increased ICP.
Unconscious/AMS with suppressed gag reflex. Conscious but unable to maintain airway. Does not prevent aspiration.
Oral Endotracheal Intubation Considerations
RA, ankylosing spondylitis, cervical fixation, Kippel-Fiel syndrome (short wide neck), thyroid or neck surgeries, Pierre Robin syndrome (small jaw, cL pallet, no gag reflex, downward displacement of tongue), Acromegaly, Epiglotitis, Tumors
Oral Endotracheal Intubation PE
- Thyro-mental distance (short< 6cm, anterior larynx, acute angle).
- LEMON, Look (obese, small, short neck, large breasts, buck teeth, receding jaw, dentures, burns, trauma, anaphylaxis, stridor), Evaluate 3-3-2, Mallampati score, Obstruction, Neck mobility
laryngoscope movement: Backward, Upward, Rward, Pressure on cartilage
Verify ET Tube Placement
Visualize passage through cords, symmetric breath sounds, no bubbling in epigastrium, symmetric chest movements, end tidal CO2 detection, condensation in tube, suction bulb, CXR
Indications for Intubation
Surgical anesthesia, comatose/GSC < 8, no gag reflex, unable to swallow spontaneously, unable to handle secretions, ventilatory failure, clinical conditions (respiratory burns, severe facial trauma, epiglottitis, large facial/neck abscesses
Indications: failed advanced airway, massive trauma, known cervical fx, upper airway obstruction. Cricothyrotomy faster and safer then tracheostomy.
Induction Agents for Intubation
- Thiopental (onset 30s, dur. 5-20min, hypotension, apnea).
- Propofol (30-60s, 4-8min, hypotension, apnea, hypertonus).
- Etomidate (30-45s, 3-12 min, myoclonus, adrenocortical suppression).
- Ketamine (30-60s, 10-15min, HTN, tachycardia, ↑ICP, hallucinations)
Paralytic Agents for Intubation
- Succinylcholine (45-60s onset, 10-12min duration, hyperkalemia, bradyarrhythmias, increased ICP, hyperthermia, etc).
- Vecuronium (2-3min, 60-80min, blocks histamine).
- Mivacurium (90-120s, 30-40min, histamine release, hypotension)
Palpate larynx, stabilize thyroid cartilage, locate cricothyroid membrane, incise skin 2-3 cm transverse and spread with hemostats, insert tracheostomy tube or small ET tube
Acute Coronary Syndromes; Aortic dissection/aneurysms; Pericarditis; Cardiac Tamponade; Hypertensive Urgency/Emergency; Pulmonary edema/CHF addressed in Respiratory Distress lecture; Arrhythmias
DDx of Chest Pain, hypotension and shock with distended neck veins
MI, cardiac arrhythmia (brady or tachy), cardiac tamponade, massive PE, tension pneumothorax
DDx of Chest Pain and Hypovolemia
MI, Aortic Dissection, leaking AAA
Pleuritic Chest Pain (worse with deep inspiration)
Pulmonary embolus, pneumothorax, pneumonia, asthma/COPD, pulmonary edema, flash pulmonary edema, pleurisy, pulmonary hypertension
Dyspnea (most common symptom- 20%), pleuritic & non-pleuritic chest pain, anxiety, cough & syncope
Pleuritic pain, tracheal deviation, hyper resonance with decreased breath sounds unilaterally – tall, thin athlete or injury – look for hyper resonance with decreased breath sounds, tracheal deviation
Pleuritic pain with associated SOB, cough, fever, sputum production, rales & dullness (infection)
Dyspnea, chest tightness, wheezing, & cough
severe respiratory distress, frothy pink or white sputum, rales, S3/S4, PND, orthopnea, edema
Flash Pulmonary Edema
- Abrupt SOB, won’t be able to lay flat.
- S3 = CHF.
- S4 = HTN (LV hypertrophy)
inflammation of pleurae, usually caused by infection or connective tissue/inflammatory dz; friction rub with low grade fever
pleuritic CP – Loud P2, R ventricular lift
GI Associated Chest Pain
Heartburn (GERD), Esophageal perforation, Mallory-Weiss, PUD, Cholecystosis, Pancreatitis
Chest pain squeezing or pressure (substernal or epigastric) exertional or @ rest, diaphoresis, radiation, N/V; post-prandial, postural, spasm & may be relieved with antacids/NTG. Innervation for heart, esophagus & stomach similar.
Presents as acute, severe, unrelenting & diffuse pain in chest, neck or abdomen (“worst pain of life”). May radiate to back or shoulders & swallowing may exacerbate pain – rare- hx w/ radiation
Hematemesis with or without prior vomiting episode
Burning epigastric pain, post-prandial sx, relieved with food, may present as N & V, wt loss, anorexia & bleeding (especially in geriatric pts)
Epigastric/RUQ “visceral” pain + fever, chills, N & V, anorexia…may radiate to back or scapular region (also cardiac eti)
Midepigastric, piercing pain, constant, radiates to back, associated with N & V, abdominal distention & exacerbation in supine position; Low- grade fever, tachycardia & hypotension may be present
Musculoskeletal Associated Chest Pain
Due to inflammation or irritation of chest wall structures is common. Sharp pain, worse with movement/palpation (also 5-10% of MI pts have reproducible chest wall tenderness…be aware!). True MS CP usually responds to NSAIDS
Anxiety/Panic Disorder Associated Chest Pain
Fleeting chest pain, variable onset/duration (usually > 30 min & persistent) & often reproducible on palpation (but not with exertion). Remember, psych pts can have MIs too!
Acute Myocardial Infarction
- ECG 10 min. CXR (portable vs PA/LAT).
- Labs: Cardiac biomarkers, (CMP), CBC, D-dimer (not specific – helpful only if very positive), PT/PTT .
- Echo: LV & valvular function, look for WMA, effusion/septal defects.
- V/Q scan versus CT (Spiral): r/o PE
- Myoglobin (1-4hr initial peak, 6-7 hrs peak, 24 hrs duration),
- CK (1-6, 12, 36),
- CK-MB (3-12, 24, 48-72),
- LDH (10, 24-48, 10-14 days),
- TnT (3-12, 12-48, 5-14 days).
- Myoglobin is not specific. Troponin is most helpful and CK-MB.
Angina Pectoris, Stable
Chest discomfort and sx from myocardial ischemia. Deep, pressure-like substernal pain, may radiate to jaw, neck, L shoulder/arm. Frequently SOB. Lasts 2-30 min. Precipitated by physical exertion or stress. Responsive to rest or SL NTG. PE often normal.
Angina Pectoris Stable (Findings)
- Findings secondary to risk factors: Elevated BP +S4, arterial bruits, AV nicking, Papilledema, cotton wool spots, Corneal arcus, Xanthelasma/Xanthomas,
- CHF +S3 (transient LV dysfunction)
- Murmurs (transient papillary muscle dysfunction, typically MR)
Angina Pectoris Labs and Imaging
- Labs: (Cardiac enzymes should be negative (CK, CKMB, Troponin) – not progressing – significant blockage but still perfusing, Elevated cholesterol, Elevated glucose)
- CXR: Often Normal; Evidence of CHF; Arterial Calcifications.
Angina Pectoris EKG
- Between episodes (1/3 have normal resting ECG or subtle non specific changes. Nonspecific ST-T wave changes–elevation=towards MI. Conduction abnormalities possible LBBB (high association with CAD), RBBB, fascicular blocks.
- During Angina (ST segment depression/possibly elevation, T wave inversion)
Angina Pectoris Tx
- Risk Factor Modifications.
- Medications: 81 – 325mg ASA daily – dose depends on other comorbidities, Beta blocker, ACE Inhibitor –(low LV fx or diabetic), Nitrates (PRN or long acting), Statins/Lipid Agents,
- Consider Revascularization (PCI/Stent vs. CABG) palliative
Acute Coronary Syndrome
Unstable angine (non ST-elevation), Non stable angina (ST elevation), Sudden cardiac death
Unstable Angina: Non STEMI
- New, sudden onset CP/pressure with associated SOB, nausea, diaphoresis. Chest Pain at greater frequency, severity or with less activity; Chest Pain at rest or nocturnally; Chest Pain previously controlled with nitrates, now refractory.
- PE: Similar to Stable Angina Exam.
- EKG similar to stable angina but more likely to show acute ischemic changes (ST depression & T wave inversion).
- Cardiac enzymes negative for USA /but elevated in NSTEMI – myocyte death.
- Tx: Admit/monitor, bed rest, MONA (Morphine, O2, NTG, ASA), Serial EKG & cardiac enzymes, ASA, Beta Blocker (slow HR), NTG (vasodilation- perfusion), ACE (LV fx, DM) & anticoagulation (heparin/LMWH vs Platelet GP IIb/IIIa Inhibitors),
- Cardiac risk stratification with cardiac catheterization preferred, Plavix (clopidogrel) following cath – if stent used
Non Stable Angina: STEMI
- 1/3 don’t survive – half deaths occur w/in first hour, 1/5 don’t recognize symptoms.
- Physical: HTN or hypotension (hypotensive= poor prognostic), Tachycardia or bradycardia, S3 (CHF)or S4 (HTN) or both, Signs of CHF (JVD elevated), Systolic murmurs (MR, VSD), Friction rub (usually day 2 or 3) – inflammation following damage.
- EKG: Helps to identify site of infarct vessel, Early Peaked T waves (0 – 6 hrs), ST segment elevation (0- 18 hrs), Q waves (takes ~ 18 hrs to “Q” out - scar) & may remain lifelong or later disappear, Extent of ST deviation & QRS duration correlate with risk of adverse outcomes.
- Acute: ST elevation at the J point in 2 or more contiguous leads, Suggestive of myocardial ischemia that may progress to MI (ST depression; T wave abnormalities).
- CLINICAL PEARL: Initial ECG is negative or non-diagnostic in up to 40% of patients having an AMI. Repeat ECG…if possible during CP episode
- Inferior MI (II, III, aVF).
- Anterior MI (V2-V5) or (V1-V4).
- Lateral MI (I, aVL, V5-V6).
- Inferolateral (II, III, aVF, I, aVL).
- Anterolateral (V4-V6, I, aVL).
- R Ventricle (R sided V1R to V6R).
- Posterior (V7 to V9).
Leads II, III, aVF. Inferior Territory/ R Coronary Artery
Leads V2-V5 or V1-V4 Anterior Territory/ L Anterior Descending
Leads I, aVL, V5-V6 L circumflex artery
Leads II, III, aVF, I, aVL
Leads V4-V6, I, aVL L main artery
R sided V1R to V6R
- Emergent PCI preferred if early presentation (< 3 hr from sx onset) & skilled team available (door to balloon time < 90 min) – in cath lab.
- Lytics within 12 hr of onset & no PCI option.
- Absolute contraindications: any prior intra-cranial hemorrhage, cerebral AVM, malignant neoplasm, active bleeding, suspected aortic dissection, ischemic CVA in past 3 months or closed head trauma, severe uncontrollable HTN.
- Tx: ASA, Beta Blockers, Oxygen, NTG +/- Morphine, ACE Inhibitors, Heparin/LMWH, GP IIb/IIIa Inhibitors, Statins, Aldosterone Inhibitors
Arrhythmias (VT, VF or heart block) electrical system affected by damage done to Myocardium, CHF/ Cardiogenic Shock (LV not able to pump), RV infarction (R coronary artery), Ventricular Free Wall Rupture, Ventricular Septal Rupture, Mural thrombus/ embolus, CVA, Pericarditis, Postinfarction angina
Sudden Cardiac Death
- Unexpected non-traumatic death in clinically well or stable patients who die within 1 hour after onset of symptoms.
- Causative rhythm is usually ventricular tachycardia except in the setting of acute ischemia or infarction (then VF arrest). Most deaths occur in the early morning hours.
- 80% contributed to coronary heart dz in Western cultures; 10-15% attributable to cardiomyopathy; 5% contributed to other rare disorders (congenital lesions, coronary artery embolism, pulmonary HTN, neoplasm, Sarcoidosis, Amyloidosis, vasculitides, LV hypertrophy disorders or conduction dz)
Severe elevation of BP. No evidence of PROGRESSIVE TOD. Benefit from BP lowering in a few hrs. Absence of raised intracranial pressure (EX: BP 190/100 with severe HA but normal neurological exam.). Patients are usually known to have HTN but have been non-adherent with meds, or treated with an inadequate regimen. Short term Rx with labetalol, clonidine or captopril with outpatient follow up within 72 hrs is recommended.
- Acute, severe elevation in BP. Evidence of rapidly PROGRESSIVE TOD (eg. MI, pulmonary edema, stroke or renal failure). Requires immediate, gradual reduction of BP (NOT to the normal range). Always look for secondary causes. (ex. BP of 240/140 with mental status changes). Acute CHF with pulmonary edema 37%. Cerebral infarction 25%. Encephalopathy 16%. MI/USA 12%. Hemorrhage –intracranial 5%. Eclampsia of pregnancy 3%. Aortic dissection 2%.
- Goal of Tx is to achieve a controlled, gradual lowering of BP. 10% decrease in first hour, then 15% over next 3 – 12 hrs to BP of no less than 160/110 mmHg. Rapid correction of BP to norm levels puts pt at high risk for worsening cerebral, renal or cardiac ischemia.
- Papilledema must be present. Usually accompanied by other end organ damage.
- Most common in young adults, prior renal dz, AA males, pregnancy, or in collagen vascular dz.
Men > women (2:1), peak incidence 60-70yo, increased risk in pregnancy and connective tissue disorder (Marfan’s, Ehlers Danlos). 80% have HTN. Increased risk if have bicuspid aortic valve or coarctation of the aorta. 95% occur in ascending aorta just distal to aortic valve or just distal to the L subclavian.
- I = ascending aorta extending to distal (entire length).
- II = ascending aorta only (before L subclavian).
- III = descending aorta only (after L subclavian)
- A = any involvement of ascending aorta.
- B = not involving ascending aorta
Sudden onset retrosternal and back pain. May see infarct pattern on ECG, neurologic deficits/CVA, limb ischemia, syncope, shock, hypertensive. Pulse discrepancies, tamponade possible. Acute AI indicates aortic root involvement
- CXR (widened mediastinum, possibly L sided pleural effusion, Widened Aortic silhouette, Widened mediastinum, L pleural effusion, 10%-20% normal).
- Echo (98% sensitive, 99% specific, +/- pericardial effusion, done bedside). CT helpful in acute presentation.
- MRA/MRI useful for serial follow up.
- EKG- LVH, non-specific or inferior abnormalities (dissections preferentially extend into R coronary ostium)
- Achieve relative hypotension & bradycardia) beta blocker first, then nitroprusside to maintain SBP of 100 -120 mmHg. Contact Cardiothoracic surgeon.
- Type A = Surgical repair, may require AVR (Aortic Valve Replacement).
- Type B = Medical therapy.
Thoracic Aortic Aneurysms
- 40% of patients are asymptomatic at Dx, symptoms dependent on size & position of aneurysm. Pain (if present) substernal, back/neck.
- Rupture: worsening of pain to severe.
- Vascular sx: CHF, ischemia, thromboembolism.
- Mass Effect: SVC syndrome (expanding aneurysm on SVC), tracheal deviation, cough, hemoptysis, dysphagia, hoarseness.
- CXR is NOT diagnostic alone (need CT or MRI if suspected & CXR-); stability of patient crucial. CXR + Must differentiate from anterior mediastinal mass (ie thymoma, lung CA).
- CT/MRI most sensitive, need coronary angiography if surgery required. No diagnostic testing should delay CT surgical consult or compromise patient.
- Large bore IV, type & cross, monitor closely.
- Acute inflammation of pericardium, usually associated with effusion ~85% associated with viral or “idiopathic” etiology; remainder are associated with TB/bacterial/fungal infections, neoplastic dz, uremia or collagen vascular dz - LUPUS, or following MI cardiac surgery or irradiation. Excessive anticoagulation can cause hemorrhagic effusion.
- SS: Pleuritic, sharp, stabbing CP that radiates to shoulders, back, neck that is worse on deep inspiration or movement, worse supine & relieved by sitting up & leaning forward.
- PE: Low grade fever, dyspnea, friction rub LLSB & sometimes palpitations or dysphagia.
- Dx: CXR typically normal, r/out other dz.
- Labs: CBC with diff, BUN/creatinine to r/out uremia, serologies (strep, ANA - lupus, viral studies), thyroid to ID underlying cause.
- Echo: may reveal effusion. Pericardiocentesis usually not necessary: Patients with tamponade, Confirm / exclude purulent pericarditis.
- Tx: Stable pts Rx as OP with NSAIDs for 1 to 3 weeks. Treat underlying cause if identified. Any pt with myocarditis, uremic pericarditis, enlarged cardiac silhouette on CXR or hemodynamic compromise should be admitted for observation.
- Tamponade occurs when the pressure in the pericardial sac exceeds normal RV filling pressure, resulting in restricted filling & decreased cardiac output.
- Etiology: TB/bacterial/fungal infections, neoplastic dz, uremia or collagen vascular dz - LUPUS, or following MI cardiac surgery or irradiation. Hours to days depending on etiology. Shortness of breath & weakness more likely than CP, tachycardia. Distended neck veins, pulsus paradoxus.
- ECG – electrical alternans an/or low voltage. Echo diagnostic for large pericardial effusion.
- CXR – not helpful unless you see a large cardiac silhouette. Although Viral Pericarditis is very common (85% of pericarditis cases) it rarely leads to tamponade.
- Conditions that may precipitate tamponade: Malignancy induced pericarditis, Aortic dissection, MI with Ventricular rupture, pacemaker perforation during implant.
- Beck’s Triad: Hypotension. Elevated systemic venous pressures, Small quiet heart.
- Tx: Tamponade is a True Emergency. Volume resuscitation, Pericardiocentesis, Admit & consider Pericardial window
Hypotension. Elevated systemic venous pressures, Small quiet heart
Mitral Valve Prolapse
Mid-systolic click, inverted T-waves inferior leads. Unclear etiology of associated chest pain.
Systolic ejection murmur transmitted to carotids. LVH on EKG
Diastolic murmur transmitted to carotid arteries, wide arterial pulse pressure, EKG may show LVH
Acute GI Bleeding Signs and Symptoms
History may suggest the source, it can be misleading. May be subtle, no obvious signs of bleeding. Mild bleeding vs hemorrhage. Hypotension, tachycardia, syncope, weakness, confusion.
Acute GI Bleeding History
Any hematemesis, coffee-ground emesis, melena, or hematochezia. Any weight loss or changes in bowel habits. Any vomiting and retching. Any history aortic graft. Any history of ASA, NSAID’s, steroids. Any ETOH abuse. Any history of iron or bismuth which can simulate melena and beets which can simulate hematochezia.
Acute GI Bleeding Physical Exam
Vital signs may show hypotension and tachycardia. Cool, clammy skin then in shock. Spider angiomata, palmer erythema, jaundice, and gynecomastia seen in liver dz. Petechiae and purpura seen in coagulopathy. Careful ENT exam to rule out causes that can mimic upper GI bleeds. Proper abdominal exam and rectal exam.
Acute GI Bleeding Labs
CBC, Electrolytes, Glucose, BUN/Creatine –BUN will be elevated in upper GI bleeds, Coagulation studies, Liver function studies, Type and cross-match
Acute GI Bleeding Diagnostics
Abdominal series - not beneficial unless specific indications. Angiography - can be diagnostic and therapeutic but requires a brisk bleed. Colonoscopy - is diagnostic and therapeutic and more accurate than bleeding scans and angiography. Endoscopy is study of choice for UGI bleed. NG tube placement recommended for all patients with GI bleeds. Negative lavage does not rule out UGI bleed.
DDX Upper Intestinal GI Bleeding
Peptic ulcer dz, Erosive gastritis, esophagitis, duodenitis (some causes are ETOH, ASA, NSAID’s), Esophageal and gastric varices (Caused by portal hypertension). Mallory-Weiss syndrome – (longitudinal tears, mucosal tear in the cardioesophageal, region, caused by repeated retching). Stress ulcers. Arteriovenous malformation. Malignancy.
- Most common cause of upper GI bleed. Duodenal ulcers 29% will rebleed in 10% of cases within 24-48hrs. Gastric ulcers 16% rebleed. Stromal ulcers < 5% rebleed.
- Prostaglandins produce mucous and bicarbonate ions which protect the tissue in the stomach by being destroyed with hydrochloric acid and pepsin.
- Dyspepsia is the imbalance between the protective mucosa and acid/pepsin. Peptic ulcer which is a defect beyond muscularis mucosa will develop if there is an imbalance. Stress ulcers do not extend through the muscularis mucosa.
- Two types of peptic ulcers:
- Duodenal ulcers which occur in the first portion of the duodenum.
- Gastric ulcers which usually occur in the lesser curvature of the stomach.
- H. pylori - a spiral, urease producing flagellated bacterium which lives between the mucus gel and mucosa. Its production of urease, cytotoxins, proteases and other compounds disturb the gel and increase tissue exposure to acid and pepsin. H. pylori is seen in 95% of patients with duodenal ulcers and 80% of gastric ulcers. Only 10-20% of patients who are infected with H. pylori will develop ulcers.
- NSAID’s - inhibit prostaglandins which in turn increases tissue exposure to acid and pepsin.
- Zollinger-Ellison syndrome - is a gastrin secreting tumor which creates such a high acid level it over rides the protective gel.
- Cigarette smoking - inhibits bicarbonate ion production and increases gastric emptying. Bile salts, Emotional stress, Type O blood, Prolonged use of corticosteroids, Caffeinated beverages. Diet and alcohol are not predisposing factors to the development of peptic ulcers.
PUD Clinical Features
- Epigastric pain - (gnawing, aching or burning) is the main complaint.
- Gastric ulcers usually develop pain shortly after eating.
- Duodenal ulcers usually develop pain 2-3 hours after eating and awaken patients at night. Pain can be relieved by food.
- Physical exam of uncomplicated PUD, there may be a finding of epigastric tenderness.
Can detect by rapid urease test, histologic study or culture during endoscopy. Serologic studies cannot be done as follow up for cure due to antibodies being present for several years after eradication of infection. Urea breath test can confirm cure. Stool antigens can be tested to confirm cure.
Stop any offending agents such as NSAID’s. Bland diets with frequent feedings have not been shown to be effective. Antacids, H2 antagonists, proton pump inhibitors, sucralfate, misoprostol, bismuth compounds,
Neutralize gastric acids. Good for acute pain relief and healing ulcers. Poor compliance due frequency of doses. Inhibit absorption of some drugs such as warfarin, digoxin, some anticonvulsants and antibiotics. Aluminum causes constipation and should not be given with renal failure patients due to accumulation which can cause osteoporosis and encephalopathy. Magnesium causes diarrhea.
Inhibit gastric acid secretion. Equally as effective as antacids with better compliance due to decreased frequency of doses. Cimetidine inhibits cytochrome p450 system greater than other H2-antagonists which will cause an increase in drugs such as warfarin, phenytoin, diazepam, propranolol, etc. Renal excretion and therefore must adjust doses in patients with renal dz.
Proton Pump Inhibitors
Inhibit gastric acid secretion. Heal ulcers faster then H2-antagonists and antacids. Omeprazole (Prilosec) has also been shown to affect the cytochrome p450 system. Lansoprazole (Prevacid) does not affect other drug metabolism. Pantoprazole (Protonix) has been shown to decrease bleeding from peptic ulcers.
Locally binds to the base of the ulcer and therefore protects it from acid. Also has been shown to absorb bile acids, inhibit pepsin activity, and increase prostaglandin production. Needs an acidic environment to work therefore not beneficial to give antacids. Causes constipation, dry mouth and inhibits the absorption of many medications.
Prostaglandin E1 analogue which acts as natural prostaglandin in the body. Only indicated for prevention of NSAID induced gastric ulcers in high risk patients. Contraindicated in pregnant women and women in childbearing age because it causes spontaneous abortion. Can cause diarrhea and crampy abdominal pain.
Bismuth Compounds (Kaopectate, Pepto-Bismol)
Decrease pepsin activity, increase mucus secretion, form a barrier protection on ulcers, augment prostaglandin synthesis, slow hydrogen ion diffusion across mucosal barrier, and H. pylori bactericidal effect. Used in triple drug combinations for the Tx of H. pylori. If H. pylori positive then must be given antibiotics to prevent recurrence of ulcer. Usually done with triple or quadruple Tx regimens. Some antibiotics in regimens are metronidazole, tetracycline, amoxicillin, clarithromycin.
Complications of PUD
- GI bleeding is the most common complication of PUD.
- Perforation: Initially a chemical peritonitis develops which then progresses to a bacterial peritonitis.
- Anterior perforation - patients will have sudden abdominal pain with guarding and rebound. 60-70% will demonstrate free air of x-rays.
- Posterior perforation - patients will develop back pain with no free air on x-ray and may mimic pancreatitis but lipase will be normal or only slightly elevated. No free air on x-rays cannot rule our perforation.
- Tx: IV fluids, electrolyte corrections, NG tube, broad spectrum antibiotics and surgery.
- Gastric outlet obstruction Scaring from healed ulcers or edema from active ulcer with development of obstruction. Obstruction will cause gastric dilation, vomiting, dehydration, metabolic alkalosis. Patients will develop upper abdominal pain with vomiting, early satiety, weight loss. Abdominal x-ray will show dilated stomach shadow with large air-fluid level. IV fluids, electrolyte corrections, NG tube, and surgery if needed.
Lower Intestinal GI Bleeding
Hemorrhoids (most common cause). Diverticulosis (common, painless, can be massive, cause from an erosion into a penetrating artery from the diverticulum). Arteriovenous malformations, CA/polyps. Inflammatory bowel dz. Infectious gastroenteritis, Meckel diverticulum.
Immediate Mgt of Acute GI Bleeding
- Large-bore intravenous lines with fluid replacement.
- Class I + II hemorrhage replace with crystalloid.
- Class III + IV hemorrhage replace with crystalloid and blood.
- NG tube should be placed and can determine upper GI from lower GI but not 100%. Also NG tubes will not worsen variceal bleeds. Foley catheter for hypotension patients to monitor output.
- Class I: 15% blood volume loss, usually no change in vitals, fluid resuscitation not necessary.
- Class II: 15-30% loss of total blood volume, often tachycardic with narrowing of pulse pressure, vasoconstriction causes pale and cool extremities, may have slight changes in behavior, volume resuscitation with NS or LR.
- Class III: 30-40% blood volume loss, BP drops, HR increases, peripheral perfusion drops (shock) and mental status worsens. Fluid resuscitation with LR and blood transfusion usually necessary.
- Class IV: > 40% blood volume loss, aggressive resuscitation is required to prevent death.
- Difficulty eating. Subjective sensation that suggest the presence of an organic abnormality in the passage of liquids or solids from the oral cavity to the stomach.
- Dysphagia is considered to be an alarm symptom –indicating the need for evaluation.
- Oropharyngeal dysphagia – arises from disorders that affect the function of the oropharynx, larynx, and upper esophageal sphincter.
- Esophageal dysphagia arises within the body of the esophagus, the lower esophageal sphincter or cardia , and is most commonly due to a mechanical causes or a motility disturbance. The cornerstone of evaluation is a careful history.
- Diagnostic Testing: Barium Swallow, Endoscopy, Esophageal Manometry, Biopsies
- Reflux esophagitis results from the combination of excessive gastroesophageal reflux of gastric juice and impaired esophageal clearance of the refluxate.
- Symptoms: chronic heartburn, regurgitations, nausea, epigastric pain.
- Causes: High Fat food, Nicotine, ETOH, Caffeine, Medications (nitrates Ca Channel Blockers, anticholinergics, progesterone, estrogen), Pregnancy.
- Tx: Mild symptomatic GERD can usually be managed empirically; lifestyle and dietary modifications along with antacids and nonprescription histamine (Zantac)– 2(H2) receptor antagonist are usually sufficient.
- Surgical: Surgical procedures include Toupet fundoplication, Hill repair and the Belsey Mark IV operation. All involve restructuring the lower esophageal sphincter to improve its strength and ability to prevent reflux. These surgeries are done less often, and their success is often dependent on the skill of the surgeon.
- Rapid Dx and therapy provide the best chance for survival – delay is common resulting in substantial mortality.
- Iatrogenic injury through esophageal instrumentation is the leading cause of perforation.
- Spontaneous rupture (Boerhaave syndrome) occurs secondary to sudden increase in intraluminal pressure – usually due to violent vomiting or retching- often preceded by heavy eating or ETOH use.
- Trauma – penetrating-blunt-caustic agents. Foreign Body, Infection, Tumor, Aortic Pathology, Barrett esophagus, Zollinger-Ellison syndrome. Mortality 5 – 75% - higher rates correlate with delays in both presentation and Dx.
- Physical Findings: Subcutaneous emphysema neck/chest – occurs in 60% of cases – but takes at least an hour to develop. Tachycardia/tachypnea. Mackler triad – vomiting – chest pain – subq emphysema. In cases of delayed presentation patients may be critically ill and present with significant hypotension.
- Esophageal varices, Mallory Weiss syndrome, Esophageal neoplastic process, Trauma. Barrett’s esophagitis – pre cancerous – metaplasia changes of esophageal mucosa.
- Dx: Endoscopy, Endoscopic ultrasound helpful to distinguish between varices and folds, Portal vein angio, Barium studies, Capsule endoscopy of the esophagus.
- Tx: Depends on severity, Broad spectrum antibiotics, NPO, NG tube, Emergent airway if indicated, Small tear – conservative approach, Larger tears – surgery – stenting-resection-drain placement, Gastric Lavage, 60% of variceal bleeding will resolve with supportive care alone. Ongoing hemorrhage can require Tx with electrocoagulation, sclerotherapy and laser photocoagulation. Angiographic embolization or surgical intervention.
Vomiting and Diarrhea
- Most often gastroenteritis.
- Viral: Norovirus (90% adults), Rotavirus (infants and children).
- Usually self-limiting. Supportive care. Dehydration danger in very young and old.
- Often food-borne or oral-fecal contamination.
- Commonly Shigella/Salmonella/E-coli/Campylobacter.
- Renal symptoms and flank pain (Pyelonephritis – UTI).
- Headache (Increase ICP, Bleed/tumor).
- Pregnancy (Hyperemeses gravidarum, Preeclampsia).
- Diabetes/Hyperglycemia (DKA).
- Cardiac (ACS).
- Prior Abdominal Surgery (obstruction, abscess formation).
- Medications (Side effects, Toxicity – lithium/digitalis/many others)
- History: Description – bloody – mucoid-watery, Frequency, Duration <2weeks – acute, >2 weeks – chronic, Associated symptoms, Recent food sources, Travel, Social hx, Occupation, Medications.
- Evaluation: Dependent upon severity/degree of dehydration, CBC, BMP, UA, Pregnancy, EKG, Rectal exam, Stool studies, Fecal WBC, C/S, Ova/parasites, C-diff.
- Tx: Antibiotics (Positive fecal WBCs, Recent travel – Cipro/Bactrim, ID hx). Anti-diarrheal agents (Imodium, Lomotil)
Acute Renal Failure
Rapidly deteriorating kidney function. Accumulation of nitrogenous waste.
Urine output < 0.5-1.0 cc/kg/hr (<400 cc/day in adults)
- Normal kidneys are hypoperfused. Hypovolemia most common cause. Dehydration (vomiting, diuretics, skin loss/burns). Ineffective circulating volumes (early sepsis, anaphylaxis, 3rd spacing—pancreatitis, peritonitis, ischemic bowel). Decreased cardiac output (CHF, MI severe).
- Tx: volume replacement to maximize cardiac output.
- Pathology of the kidney.
- Tubulointerstitial: acute interstitial nephritis/tubular necrosis due to drugs, infection, ischemia, nephrotoxins, rhabdomyolysis.
- Glomerular: postinfective glomerulonephritis (GABHS, 1-3 wks after pharyngitis or impetigo, pneumococcus, staphylococcus, SLE, vasculitis, Henoch-Schönlein purpura).
- Vascular: thrombosis, TTP/DIC, NSAID overdose, severe HTN, HUS.
- Tx: fix pump or replace it. Low dose dopamine. Mannitol in early rhabdomyolysis. Dialysis.
Urine outflow obstruction. Ureteral or bladder obstruction from kidney stones, blood clots, malignancies, prostatic hypertrophy. Urethral obstruction from strictures, phimosis or meatal stenosis.
ARF Labs and imaging
- BMP, BUN (>20), Cr (>1.4), BUN:CR ratio (10:1 normal, 20:1 prerenal), Electrolytes, UA (RBC, casts).
- Renal/bladder US for hydronephrosis and postvoid residual. CT non-contrast for stones.
- Tx: relieve obstruction, foley, ureteral stent, nephrostomy
Cystitis and Pyelonephritis
Females > Males, extremes of age
Older men, BPH
- Dysuria, frequency, urgency, hematuria, urethral discharge, pain (suprapubic, rectal, costovertebral).
- UA: dip (leukocyte esterase), microscopic (WBC, RBC, bacteria, squamous epithelial cells, trich, yeast).
- Pathogens: E-coli most common, Klebsiella, Proteus, Enterobacter, Pseudomonas.
- Tx: sulfonamides, fluoroquinolones, nitrofurantoin (safe in pregnancy), patient education.
- Uncomplicated Tx for 3 days.
- Complicated Tx for 7-14 days (pyelonephritis, pregnant, male, frequent UTIs, prior Tx failure.
- Culture: pyelonephritis, resistant or recurrent UTIs, men.
- DDx: vaginitis (yeast, BV), foreign body (peds), HSV, cervicitis, PID (green/yellow discharge, pelvic exam)
- Sources: gonorrhea, chlamydia, trichomonas, herpes simplex.
- Symptoms may improve if untreated but may be able to transmit and risk of stricture and disseminated dz.
- Tx: Gonorrhea (Ceftriaxone/Rocephin IM), Chlamydia (Azithromycin or Doxycycline), Trichomonas (Metronidazole/Flagyl). All sexual partners should be treated.
- Irritative voiding symptoms, malaise, fever, chills, back or rectal pain. Painful, firm, swollen prostate (do not massage prostate to avoid spreading infection).
- < 35yo (GC/Chlamydia).
- > 35yo E-coli, Klebsiella, Enterobacter, Proteus.
- Tx: Ceftriaxone, Quinolone, TMP/Sulfamethoxazole (Bactrim)
- Calcium oxalate or phosphate stones (75%), magnesium ammonium phosphate (15%), uric acid/cystine associated with gout.
- SS: flank pain, abrupt onset, N/V, previous episodes.
- PE: CVA tenderness, lower quadrant abdominal pain.
- DDx: AAA, appendicitis, tuboovarian abscess, ectopic pregnancy.
- Dx: noncontrast CT, US (hydronephrosis and maybe stones), KUB.
- Tx: IV hydration, aggressive pain mgt (narcotics, NSAIDs, oral fluids, Flomax).
- Admission criteria: infection/sepsis, complete obstruction, deteriorating renal function, intractable N/V, solitary kidney, very large or proximal stones.
- Urologic emergency.
- Young men < 30. Abrupt onset after exertion or during sleep.
- Severe nonpositional pain, low abdominal, inguinal canal, scrotum. N/V. absence of cremasteric reflex.
- Infection and inflammation.
- GC/Gonorrhea (< 35). E-coli,
- Enterobacter, pseudomonas (> 35).
- Prehn’s sign unreliable (pain relief with elevation of testicle).
- Gradual onset. Unilateral pain and swelling. Fever, dysuria, local tenderness.
- Tx: analgesics, testicular support, stool softeners, antibiotics.
Abnormally dilated testicular veins (bag of worms). Usually asymptomatic. Mass separate from testis. Increases with valsalva.
Gradually enlarging, painless, transilluminates. Aspiration clear fluid. US helpful.
Asymptomatic mass, separate from and superior to testicle. Aspiration white cloudy fluid. US helpful.
Incarcerated Inguinal Hernia
Trapped in scrotum. Bowel sounds heart.
Loss of blood supply. Surgical emergency.
Young men, asymptomatic enlargement, firm/nontender mass that does not transilluminate, US helpful. Surgical exploration necessary for exact Dx.
History of injury, scrotal hematoma, blood at urethral meatus, US, urology consult.
- Painful sustained erection usually unrelated to stimulation.
- Associated with Sickle Cell dz.
- Occasional side effect of erectile dysfunction medications.
- Decreased venous flow (ischemia, unable to urinate).
- Urologic emergency.
- Necrotizing fasciitis. Potentially life threatening. Polymicrobial.
- Risk factors: DM, ETOH, obesity.
- Urology/surgical consult.
- Abx (Ampicillin, Clindamycin).
- Manage shock or sepsis.
Inability to retract foreskin, fibrous constriction or scar.
- Inability to reduce retracted foreskin over the glans.
- Emergent Tx. Continuous firm pressure 5-10min and attempt to reduce, dorsal slit with local anesthetic.
- Circumcision is definitive therapy.
- Clinical: Recurrent infection. Classic sign of gonorrhea is very purulent.
- DD: Chlamydia, gonorrhea, treat both! Kids almost always bacterial Gonorrhea can penetrate into intact cornea!
- Rx: controversial – other ophthalmic conditions?
- Clinical: red eyes & d/c; Usually adenovirus. Pull down eyelid and you see little clumps.
- DD: Bacteria or viral, In adults – almost always viral.
- Rx: no curative Rx. Supportive care. Clean everything. Throw out contact lens case and solution. Wash sheets and towels. Wash hands religiously. Contagious for 2 weeks. Stay out of contacts until better.
Hordeolum, Chalazion, Stye
- Hordeolum is acute (usually red).
- Chalazion is chronic (often fibrotic). Both represent clogged oil glands.
- Stye = all of the above. Can be painful; cosmetic; can affect vision.
- Rx: Initially, treat conservatively. Warm compresses. Erythromycin ointment. May need I&D. Steroids sometimes injected to prevent recurrence. Routine warm compresses for prevention.
- Clinical: Inflammation along the eyelashes/meibomian glands. Different varieties, but generally represents clogged meibomian glands and altered balance of normal bacterial flora of the lids.
- Rx: Treat with warm compresses, lid scrubs. Consider erythromycin ointment or doxycycline. If ulceration or lass loss present, consider cancer.
- Clinical: Inflammation and bacterial superinfection of the lacrimal sac will cause dacryocystitis. Common pathogens are Streptococcus pneumoniae, Staphylococcus aureus, S. epidermidis, Haemophilus influenzae, and S. agalactiae. Infants develop a chronic mucopurulent discharge followed by erythema and swelling inframedially to the eye. In children of all ages, dacryocystitis is usually a sequal of bacterial superinfection after a viral upper respiratory infection.
- The Dx is made when gentle pressure with a finger tip or cotton swab applied to the nasolacrimal sac causes a reflux of mucopurulent material. Culture the discharge to identify the causative agent.
- DD: bacterial conjunctivitis, canaliculitis, dry eye syndrome, eye abrasion, lacrimal sac obstruction.
- Rx: Improperly treated dacryocystitis may lead to periorbital and orbital cellulitis. Parenteral antibiotic therapy is required for ill- or toxic-appearing children.
- Clinical: Almost always a post-operative condition; trauma; can happen endogenously but not common. Be aware of a red eye in any patient with recent eye surgery or a history of glaucoma surgery ever in the past.
- True ocular emergency: needs an injection of intravitreal antibiotics or surgery ASAP, visual outcome depends on how quickly they can get antibiotics.
- Hypopyon (pus in the eye) infected hyphema.
- Source: coag neg staph, staph, gram negatives- less common.
- Rx: inject antibiotics fast!
- History: Skin wound; Sinus dz.
- Work-up: Eye exam: Motility, Pupils, CT.
- Tx: PO or IV antibiotics
- Clinical: white spot on cornea.
- DD: focal loss of stroma w/ overlying epithelial defect- infectious or non-infectious.
- RF: contact lens wearers – sleeping in them, swimming; trauma; eyelid structural abnormality; chronic epithelial dz (severe dry eye); immunosuppression.
- Agents: Bacteria, virus, fungus, protozoa. If suspicious, call an ophthalmologist.
- Work-up: bacterial, fungal and viral cultures.
- Tx: broad-spectrum antibiotic drops. Follow-up: daily.
Conjunctival Hemorrhage and Abrasion
The conjunctiva has less innervation than the cornea, so conjunctival abrasions are far less symptomatic than corneal abrasions. The patient may complain of a scratchy foreign body sensation, mild pain, tearing, and, rarely, photophobia. Vision should not be affected unless there is a full-thickness conjunctival laceration with associated penetration of the globe. Physical examination may reveal mild conjunctival injection, and, occasionally, subconjunctival hemorrhage. A conjunctival abrasion may be invisible without fluorescein staining. Conjunctival lacerations have a presentation similar to conjunctival abrasions and should be relatively asymptomatic. Evert the upper eyelid and inspect under the highest magnification available to avoid missing any additional foreign bodies. Frequently, small wooden particles such as sawdust will blend into the conjunctiva when moistened by the tears and be difficult to find without slit lamp magnification.
- Symptoms: Sharp pain/foreign body sensation, photophobia, tearing.
- Signs: White corneal infiltrate develops. Fluorescein staining, conjunctival injection, swollen lid. After dye – cobalt blue light.
- DD: Dry eye/recurrent erosion syndrome, infectious keratitis (bacterial ulcer, HSV, acanthamoeba, fungal ulcer).
- Work-up: Slit-lamp exam with fluorescein. Evert lids to rule out foreign body.
- Tx: Noncontact lens wearer: antiobiotic ointment or drops (erythromycin, polytrim, etc.). Contact lens wearer: must cover pseudomonas (tobramycin ointment, fluoroquinolone drop). Cycloplegic agent (homatropine, scopolamine). Consider patching or bandage contact lens.
- Follow-up in 24 hours. Refer to an ophthalmologist if not healed in 24 hours
Determine mechanism of injury. Rule out open globe or other ocular injury. Consider tetanus. Determine extent of injury. Remove foreign bodies. Status of lid margin – line up lid margins when sewing. Status of orbital septum/levator aponeurosis – orbital fat should be behind. Status of lacrimal drainage apparatus.
- Symptoms: Pain, blurred vision, history of blunt trauma.
- Signs: Blood in anterior chamber.
- Hyphema: blood layers out and is grossly visible.
- Microhyphema: RBC’s floating in anterior chamber.
- Work-up: Assume open globe. Complete eye exam to r/o open globe. Consider CT scan for open globe/blow-out fracture. Consider Ultrasound to r/o vitreous hemorrhage or retinal detachment. Serum protein electrophoresis in patients at risk for sickle cell anemia.
- Tx: Consider hospitalization (controversial). Shield eye (no patch). Bedrest with bathroom privileges. Head of bed elevated to 30 degrees. Topical Atropine. No aspirin or NSAID’s. Consider topical steroid. Monitor intraocular pressure and treat as necessary –RBCs not good for internal drain
Trauma. Requires full eye exam. Consider prophylactic antibiotics. Consider exam by Eye MD/ENT/Plastics. Some require urgent repair (dramatic enophthalmos, entrapment of extraocular muscles) , wait a few weeks to see. Many will improve as swelling resolves. Consider ice packs.
- Symptoms: Pain, Decreased vision. Signs: 360 degrees of subconjunctival hemorrhage, Corneal or scleral laceration, Intraocular contents outside the globe, Hyphema, Low intraocular pressure.
- Work-up: DO NOT PRESS ON THE EYE, Obtain what exam is possible, Consider CT scan or Ultrasound to evaluate contour of globe, location of lens, presence of retinal detachment and presence of intraocular foreign body. Initial
- Tx: protect the eye, NPO, IV antibiotics, Tetanus toxoid if needed, Antiemetic, Bedrest, Plan surgical repair
Acute Angle Closure Glaucoma
- Internal fluid made by ciliary should drain into internal drain – fluid gets stuck; pressure builds behind iris – closes angle.
- RF: More in Asians, women, far sighted, age, movie theater (mid dilated position), anticholinergics, cataract surgery.
- Symptoms: Severe pain, red eye, halo around lights, decreasing vision, v/v ab pain.
- PE: Slit lamp – how deep angle is.
- Tx: Lower eye pressure:
- Drops: timolol, dorzolamide, brimonidine.
- Oral agents: diamox, isosorbide.
- IV agents: mannitol. Laser to make a hole in iris so fluid can drain. Can prophylactically be done to other eye
Central Retinal Artery or Vein Occlusion
- Temporary loss of vision that does not go away – sudden loss of vision
- PE: Cherry red spot in macula; plaque on artery.
- Work-up: ESR(sed rate and maybe c reactive protein) for Temporal Arteritis (vasculitic dz- if it is can happen to other eye).
- Tx: Call ophthalmologist. No Tx is proven to improve outcome.
- Can try: lowering intraocular pressure with topical meds, diamox, anterior chamber paracentesis, maybe will move embolism downstream. @ duke- TPA in interventional radiology (contraindications, w/in 3 hrs)
- Risk factors: Myopia, Trauma, Family history, Cataract surgery, RD in the fellow eye. History: Flashes or floaters, new ones.
- Exam: Vision may be 20/20, Confrontational visual fields may reveal a defect – loss of visual fields , Eye pressure may be lower in affected eye.
- Rx: Surgery – ocular urgency!
- Typical optic neuritis occurs in young women and is accompanied by painful eye movements.
- Associated with multiple sclerosis.
- Exam: May or may not show optic nerve head swelling, Visual field, Color vision, Pupils.
- Tx: ophthalmology and neurology, Not PO steroids, Maybe IV steroids, Maybe interferon, Consult
Giant Cell Arteritis (Temporal Arteritis)
- Systemic dz which can result in permanent vision loss.
- History: Usually older than 70 years, Jaw claudication, Tender over temporal artery, Weight loss/fevers.
- Dx: Check ESR and CRP.
- Tx: If suspicious, consider PO steroids and temporal artery biopsy.
- Iritis is inflammation of the anterior segment of the uveal tract. Not a true ocular emergency, but does require follow-up by an ophthalmologist.
- Pain in iritis is caused by irritation of the ciliary nerves and ciliary muscle spasm. Ciliary spasm irritates the trigeminal nerve and can cause photophobia. WBCs released from the uveal vessels may be seen in the anterior chamber with the slit lamp and are termed cells (as in "flare and cells"). Cells appear as snowflakes in a headlight beam at night.
- Clinical Features: unilateral pain, although the pain may be bilateral with systemic dz. There may be complaints of conjunctival injection, photophobia, and decreased vision. There is usually no discharge.
- Complaints of systemic symptoms, including arthritis, urethritis, and recurrent GI symptoms, are not unusual. Past medical history should include exposure to tuberculosis, history of genital herpes, or history of previous similar symptoms, and the associated Dx.
- Ask about recent trauma or exposure to welding without protective goggles.
- Exam: Inspection of the eye may reveal a perilimbal flush (injection is greatest around the limbus) or diffuse conjunctival injection without mucopurulent discharge. Photophobia is usually present. Consensual photophobia (shining light on the unaffected eye causes pain in the affected eye) is highly suggestive of iritis. The pupil is usually miotic poorly reactive. Visual acuity may be decreased with severe inflammation and clouding of the aqueous humor. Slit lamp examination will reveal flare and cells in the anterior chamber, culminating in a hypopyon with severe dz. Anterior or posterior synechiae may occur with chronic dz. intraocular pressure may be decreased if the ciliary body is involved secondary to decreased production of aqueous humor. Fluorescein staining of the cornea may show abrasions, ulcerations, or dendritic lesions.
- DDx: Systemic dzs: juvenile rheumatoid arthritis, ankylosing spondylitis, ulcerative colitis, Reiter syndrome, Behçet syndrome, Sarcoidosis. Infectious: TB, Lyme dz, Herpes simplex, Toxoplasmosis, Varicella zoster, Syphilis, Adenovirus. Malignancies: Leukemia, lymphoma, malignant melanoma. Trauma/environmental: corneal foreign body, post-traumatic, ultraviolet keratitis.
- Tx: Tx is aimed at reducing inflammation and preventing complications such as posterior synechiae. Ophthalmologic evaluation is needed to establish the Dx and institute Tx.
- True ocular emergency. Immediate irrigation before arrival to ER. Do no try to neutralize pH by adding acid to alkali or vice versa.
- Rx: Start irrigation IMMEDIATELY, before checking visual acuity. Instill topical anesthetic. Check for and remove foreign bodies. Institute copious irrigation using Morgan contact lens if available. Once irrigation is running obtain more history and call ophthalmology. After irrigating for 30 min, check tear pH, if not 7, continue irrigation. If pH remains abnormal sweep fornices for particulate matter. Instill topical cycloplegic and topical antibiotic.
POC US also known as point-of-care limited ultrasound (PLUS)
US brought to the patient and performed by the provider in real time. Images can be obtained nearly immediately, and the clinician can use real-time dynamic images (rather than images recorded by a sonographer and interpreted later), allowing findings to be directly correlated with the patient's presenting signs and symptoms. easily repeatable if the patient's condition changes
POC US Procedural Benefits
May improve success and decrease complications in procedures performed by multiple specialties, including central and peripheral vascular access, thoracentesis, paracentesis, arthrocentesis, regional anesthesia, incision and drainage of abscesses, localization and removal of foreign bodies, lumbar puncture, biopsies, and other procedures. Procedural guidance may be static or dynamic. With static guidance, the structure of interest is identified, and the angle required by the needle is noted, with the point of entry marked on the skin. In dynamic procedures, ultrasonography visualizes the needle in real time. Static guidance may initially be easier to perform, but properly performed dynamic guidance provides more accurate guidance and is generally preferred by experienced users. Use of ultrasound to guide central venous access has been shown to reduce the failure rate, the risk of complications, and the number of attempts.
POC US Diagnostics
May involve the use of a series of focused ultrasonographic examinations to efficiently diagnose or rule out certain conditions in patients presenting with particular symptoms or signs, such as hypotension, chest pain, or dyspnea. FAST scan.
POC US Pneumothorax
In a normal lung, the visceral and parietal pleura are closely associated, and ultrasound shows shimmering or sliding at the pleural interface during respiration. The absence of sliding indicates a pneumothorax. US has been shown to be more accurate than auscultation or chest radiography for the detection of pleural effusion, consolidation, and alveolar interstitial syndrome in the critical care setting
POC US Screening
Noninvasive and lacks ionizing radiation. Screening test for cardiovascular and gynecologic disease. Benefits of screening must be weighed against the harms, particularly false positive findings that lead to unnecessary testing, intervention, or both. USPSTF has specifically recommended that ultrasonography not be used for routine screening for carotid stenosis, peripheral vascular disease, or ovarian cancer in the general population. USPSTF gave class B recommendation for one-time ultrasound screening for abdominal aortic aneurysm in men between the ages of 65 and 75 years who had ever smoked.
US FAST scan
FAST (focused assessment with sonography for trauma): integrated, goal-directed, bedside examination to detect fluid, which is likely to be hemorrhage in cases of trauma. Allows immediate, dynamic, and repeated assessments in these situations and has the potential for detecting conditions such as pneumothorax in which ultrasonography was traditionally thought to be unhelpful. May be completed in less than 5 min and has been shown to have a sensitivity of 73 to 99%, a specificity of 94 to 98%, and an overall accuracy of 90 to 98% for clinically significant intraabdominal injury in trauma. Has been shown to reduce the need for CT or diagnostic peritoneal lavage and to reduce the time to appropriate intervention, resulting in a shorter hospital stay, lower costs, and lower overall mortality
Extended FAST (e-FAST) also includes examination of the chest for pneumothorax. e-FAST examination combines five focused examinations for the detection of: free intraperitoneal fluid, free fluid in the pelvis, pericardial fluid, pleural effusion, and pneumothorax. Peritoneal fluid is detected using views of the hepatorenal space (Morison's pouch), splenorenal space, and retrovesicular spaces. The thorax is evaluated for fluid at the flanks and for pneumothorax anteriorly. The pericardium may be evaluated for effusion, particularly in cases of penetrating trauma. For assessing patients with trauma for pneumothorax, ultrasonography has been shown to be more than twice as sensitive as conventional supine chest radiography for detecting occult pneumothorax (pneumothorax seen only on CT), with similarly high specificity (>98%)
US for DVT
- Indications: Pain, Swelling, Erythema, Fail well criteria, D-dimer elevated
- Virchow’s triad: stasis, endothelial injury, hypercoagulability
- Positive Homan’s test
- Pratts sign
- Diagnosis: non-compressible, poor augmentation, hyperechoic (older), hypoechoic (fresh)