All templates are in alphabetical order, at least grouped by first letter.
A
# AKI, attributable to hypovolemia/poor fluid status
# AKI Stage 1, attributable to hypovolemia/poor fluid status
# AKI Stage 2, attributable to hypovolemia/poor fluid status
# AKI Stage 3, attributable to hypovolemia/poor fluid status
– Baseline sCr (BCr):
– Last sCr documented prior to admission:
– Stage 1: Cr > 1.5-1.9 * BCr, OR incr >0.3, OR UOP <0.5 mL/kg/hr for 6-12 hrs
– Stage 2: Cr > 2.0-2.9 * BCr, OR UOP <0.5 for >11hrs
– Stage 3: Cr > 3 * BCr, OR incr >3.9 BCr, OR anuria for >11hrs
PLAN
– NO indications for emergency KRT (NO K>6.5, NO uremic symptoms) NO refractory pulmonary edema
– NO contraindicated medications: NO NSAIDs, NO ACEis, NO ARBs, NO iodinated contrast agents
– AKI attributable to hypovolemia/poor fluid status (w/ NO signs of pulm edema, anuria), so IVF
– 1L LR IV QD
# Stage 3 Acute Kidney Injury (AKI)
– AKI Stage 3: In ER, Pt w/ rapid ↑ in sCr >3.0 mg/dL or ↑ by ≥4x baseline, ↓ urine output <0.3 mL/kg/hr for ≥24 hrs or anuria for 12 hrs
– Risk factors: Pre-existing CKD, advanced age, DM, HTN, exposure to nephrotoxins
– Complications: Volume overload, hyperkalemia, metabolic acidosis, uremia, increased risk of infections, prolonged hospital stay, potential need for renal replacement therapy
– Red flags: Oliguria, progressive ↑ sCr, persistent hyperkalemia, severe acidosis
— Diagnostic criteria: Random cortisol <3 mcg/dL OR inappropriately low cortisol response (<18 mcg/dL) after ACTH stimulation test (cosyntropin); primary adrenal insufficiency suggested by concurrent elevated ACTH, low aldosterone, and hyponatremia/hyperkalemia; secondary adrenal insufficiency suggested by low ACTH
— Potential complications: adrenal crisis (hypotension, shock, death), severe hypoglycemia, hyponatremia, hyperkalemia, metabolic acidosis
— Impact on management of other diseases: complicates sepsis management (may mimic septic shock), affects glucose control in DM, alters response to stress (surgery, trauma, infection)
— Red-flag findings: hypotension refractory to fluids/vasopressors, severe hypoglycemia, profound hyponatremia (sNa <120), hyperkalemia (>6.0), LOC/AMS
— Reassuring findings: appropriate cortisol rise on ACTH stim test, normal sNa/sK w/ therapy, stable BP w/o vasopressor requirement
PLAN
— Diagnostics
— In acute adrenal crisis:
— Hydrocortisone 100 mg IV STAT, then 50 mg IV Q6H or 200 mg/24h continuous
— IVF resuscitation w/ NS 1-3L as needed
— Dextrose 5% infusion if hypoglycemia
— If no acute crisis but suspected adrenal insufficiency:
— Hydrocortisone 15-25 mg/day divided BID (e.g., 15 mg AM, 5 mg PM) pending testing
— Mineralocorticoid replacement (if primary adrenal insufficiency):
— Fludrocortisone 0.05-0.2 mg PO QD titrated for BP, sNa, sK
— Stress-dose steroids:
— Minor procedures: hydrocortisone 25 mg IV pre-procedure
— Moderate stress: hydrocortisone 50-75 mg IV daily divided Q8H
— Major stress (e.g., major surgery, sepsis): hydrocortisone 100-150 mg IV daily divided Q8H
— Supportive care:
— D50 IV bolus if BG <60
— Electrolyte repletion (sNa >130, sK <5.0)
— Monitor glucose Q6H and electrolytes Q6-8H until stable, then daily
— Chronic management:
— Maintenance hydrocortisone as above
— Stress-dose education (double/triple dose during illness)
— Endocrinology consultation
— Monitoring:
— sNa, sK, glucose Q6H initially, daily after stabilization
— Vital signs Q1H in crisis, then Q4H
— Expected duration:
— Acute crisis stabilizes within 24-48h
— Lifelong glucocorticoid ± mineralocorticoid replacement for primary adrenal insufficiency
# Anaphylaxis in Setting of Gadolinium MRI (Anaphylactic reaction to contrast agent, Allergic reaction to gadolinium, Hypersensitivity reaction to MRI contrast)
– HPI: In ER, pt presented w/ sudden onset of urticaria, facial edema, dyspnea, and hypotension w/in minutes post gadolinium contrast for MRI. No known allergies to gadolinium. No prior similar reactions.
– Risk factors: Atopy, prior contrast reactions, shellfish allergy (debated relevance).
– Exam findings: Tachycardia, wheezing, hypoxemia, angioedema.
– Ddx: Vasovagal reaction, contrast-induced nephropathy, mastocytosis, other allergic reactions.
PLAN
– Immediate intervention:
– IM epinephrine 0.3-0.5 mg (1:1000) STAT, repeat PRN q5-15min.
– High-flow O2, monitor SpO2.
– IV fluids: NS bolus 1-2 L, continue based on BP.
– Additional Rx:
– Diphenhydramine 25-50 mg IV/IM.
– Ranitidine 50 mg IV.
– Methylprednisolone 125 mg IV (consider if no immediate improvement w/ epi).
– Monitoring:
– Continuous cardiac and BP monitoring.
– Q15min vitals until stabilization.
– Labs:
– CBC, CMP, tryptase (post 1-2 hrs of reaction onset).
– Post-stabilization:
– Observation for min 6-8 hrs for biphasic reaction.
– Consider ICU if severe or protracted course.
– Discharge planning:
– EpiPen Rx and education.
– Allergy follow-up for possible desensitization.
– Alternative contrast consideration for future imaging.
– Avoidance of future exposure to gadolinium-based contrasts.
– Note: Steroids (e.g., methylprednisolone) are adjunctive, not primary therapy. Indicated for persistent symptoms despite epinephrine and antihistamine treatment or in cases of biphasic anaphylaxis.
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FURTHER CONSIDERATIONS
In the case of a patient who is now stable after an anaphylactic event and has been treated with epinephrine, diphenhydramine (Benadryl), and methylprednisolone, it’s important to closely monitor their clinical status, especially if they are now requiring supplemental oxygen. The new oxygen requirement could indicate a possible progression of airway involvement or other complications.
Here are some steps to consider:
1. **Continuous Monitoring**: Vital signs, oxygen saturation, respiratory status, and clinical appearance should be continuously monitored. Look for any signs of deterioration or improvement.
2. **Respiratory Support**: If the patient is requiring oxygen, assess whether the current level of support is adequate. Consider escalating respiratory support if there is evidence of worsening respiratory status.
3. **Re-evaluation of Airway**: In anaphylaxis, there’s a risk of airway edema. If there are signs of airway compromise (stridor, hoarseness, or worsening respiratory distress), further intervention may be necessary.
4. **Repeat Dosing of Medications**: Depending on the time elapsed since the initial treatment and the patient’s response, consider repeat dosing of antihistamines, steroids, or epinephrine as clinically indicated.
5. **Consideration for Bronchodilators**: If there are signs of bronchospasm, such as wheezing, bronchodilators (e.g., albuterol) may be indicated.
6. **Fluid Resuscitation**: Ensure adequate hydration and perfusion, as anaphylaxis can lead to significant fluid shifts.
7. **Observation Period**: Patients with anaphylaxis, especially those who have required significant intervention, should be observed for an extended period due to the risk of biphasic reactions.
8. **Further Investigations**: Depending on the clinical scenario, further investigations (like chest X-ray, blood gases, or complete blood count) might be necessary to rule out other causes of respiratory distress or complications.
9. **Allergist Referral**: Following recovery, referral to an allergist for further evaluation and avoidance strategies is crucial.
10. **Patient Education**: Before discharge, educate the patient and their family about recognizing and managing anaphylaxis, including the use of epinephrine auto-injectors.
Each case of anaphylaxis can present differently, and decisions should be tailored to the individual patient’s clinical presentation and response to initial treatment. Collaboration with a multidisciplinary team, including potentially intensive care specialists, can be valuable in managing complex cases.
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# Pulmonary Edema
# Acute Heart Failure (AHF), Cardiogenic Pulmonary Edema, Hypertensive Emergency
– In ER, pt presented w/ acute SOB, orthopnea, PND; Hx of HTN, prior CHF episodes
– Physical exam: B/L rales, wheezing, tachypnea, JVD; use of accessory muscles for breathing
– CXR: B/L alveolar infiltrates, Kerley B lines, cardiomegaly
– BNP elevated; sCr and electrolytes w/in normal range
– EKG: LVH, possible old MI
– Echo: Reduced EF, possible diastolic dysfunction, high pulmonary artery pressures
Dx Criteria: AHF based on clinical presentation (SOB, orthopnea, PND), physical exam findings (rales, wheezing, JVD), imaging (CXR findings), and lab results (elevated BNP, EKG, Echo findings)
PLAN
– Stabilization and Monitoring
– High-flow O2 therapy or NIPPV for respiratory distress
– Continuous cardiac and hemodynamic monitoring
– IV access for rapid medication administration and fluid management
– Frequent vitals: Q1H for first 4-6H, then Q2H
– Diuretic Therapy:
– IV furosemide (Lasix) 20-40mg initial dose, titrate per response; max 160mg Q6H
– Monitor UOP, target >100 mL/hr
– Daily weights for fluid balance assessment
– Vasodilator Therapy:
– IV nitroglycerin if systolic BP >110 mmHg, titrate for symptom relief and BP control
– Inotropic Support (if hypotensive):
– Dobutamine or milrinone infusion, titrate to BP and clinical response
– ACEi/ARBs/ARNI, Beta-blockers, aldosterone antagonists if BP allows
– Consider noninvasive or invasive mechanical ventilation if severe respiratory distress
– Electrolyte Repletion:
– Monitor and replete K, Mg, Ca as needed
– Continuous cardiac enzyme monitoring: troponins Q6H for 24H
– Consider pulmonary artery catheterization in refractory cases
– DVT Prophylaxis:
– LMWH or UFH as per hospital protocol
– Nutritional support as tolerated, preferably oral; NPO if severe respiratory distress
Complications to monitor for:
– Flash pulmonary edema
– Cardiogenic shock
– Acute kidney injury
– Arrhythmias (esp. atrial fibrillation)
– Secondary infections (e.g., pneumonia)
Red-flag symptoms:
– Rapid escalation of O2 requirements
– Hypotension despite therapy
– Rising sCr or oliguria
– Worsening acidosis on ABGs
Interactions with other conditions:
– Careful fluid management in renal impairment
– Adjust medications in liver impairment
– Monitor closely for ischemic events in known CAD
– Consider impact of beta-blockers in COPD/asthma
Reassuring findings:
– Improved respiratory status with O2 therapy
– Reduction in JVD, rales with diuresis
– Stabilization of hemodynamics
– Improved UOP
Treatment duration:
– Acute phase: Continuous monitoring and therapy adjustments in first 24-48H
– Transition to oral diuretics and vasodilators as condition stabilizes
– Consider long-term therapy adjustments based on EF and overall cardiac functio
# Cardiogenic Shock (Acute myocardial infarction, Acute and subacute ischemic heart disease, Cardiac arrhythmia)
– In ER, pt presented w/ hypotension (BP 80/50 mmHg), altered mental status, cool extremities
– Hx of CAD, recent chest pain; EKG shows ST elevations
– Differential diagnosis: myocardial infarction, arrhythmia, acute valvular dysfunction, exacerbation of chronic heart failure
– New-onset arrhythmias as potential cause: atrial fibrillation with RVR, ventricular tachycardia
PLAN
– Lab orders: CBC, CMP, troponin, BNP, ABG, lactic acid, coagulation profile
– Imaging: Echocardiogram, CXR
– Continuous EKG monitoring for arrhythmia detection
– (1) Hemodynamic stabilization:
– IV fluids bolus (NS or LR) 500 mL, reassess after each bolus
– Vasopressors (e.g., norepinephrine or dopamine) to maintain MAP >65 mmHg
– Inotropes (e.g., dobutamine) if evidence of poor perfusion despite adequate fluid resuscitation
– (2) Urgent coronary angiography if MI suspected
– (3) Arrhythmia management:
– Careful assessment of hemodynamic status to guide arrhythmia management
– Consider electrical cardioversion for unstable tachyarrhythmias
– If VT: Amiodarone IV, consideration for electrical cardioversion if hemodynamically unstable
– Avoid negative inotropes (e.g., metoprolol, diltiazem) in the setting of cardiogenic shock
– (4) Mechanical circulatory support if refractory to medical therapy:
– Intra-aortic balloon pump (IABP)
– Extracorporeal membrane oxygenation (ECMO) as a bridge to decision/recovery
– (5) Additional considerations:
– Treat underlying cause (e.g., revascularization for MI, valve repair for acute valvular dysfunction)
– Monitor urine output, renal function
– Serial ABGs and lactic acid to assess for ongoing ischemia or metabolic derangements
# Cardiogenic Shock (Acute myocardial infarction, Acute and subacute ischemic heart disease, Cardiac arrhythmia)
– In ER, pt presented w/ hypotension (BP 80/50 mmHg), altered mental status, cool extremities
– Hx of CAD, recent chest pain; EKG shows ST elevations
– Differential diagnosis: myocardial infarction, arrhythmia, acute valvular dysfunction, exacerbation of chronic heart failure
– New-onset arrhythmias as potential cause: atrial fibrillation with RVR, ventricular tachycardia
PLAN
– Lab orders: CBC, CMP, troponin, BNP, ABG, lactic acid, coagulation profile
– Imaging: Echocardiogram, CXR
– Continuous EKG monitoring for arrhythmia detection
– (1) Hemodynamic stabilization:
– IV fluids bolus (NS or LR) 500 mL, reassess after each bolus
– Vasopressors (e.g., norepinephrine or dopamine) to maintain MAP >65 mmHg
– Inotropes (e.g., dobutamine) if evidence of poor perfusion despite adequate fluid resuscitation
– (2) Urgent coronary angiography if MI suspected
– (3) Arrhythmia management:
– If AF with RVR: Rate control (e.g., metoprolol, diltiazem) and consideration for cardioversion
– If VT: Amiodarone IV, consideration for electrical cardioversion if hemodynamically unstable
– (4) Mechanical circulatory support if refractory to medical therapy:
– Intra-aortic balloon pump (IABP)
– Extracorporeal membrane oxygenation (ECMO) as a bridge to decision/recovery
– (5) Additional considerations:
– Treat underlying cause (e.g., revascularization for MI, valve repair for acute valvular dysfunction)
– Monitor urine output, renal function
– Serial ABGs and lactic acid to assess for ongoing ischemia or metabolic derangements
– (6) Follow-up and secondary prevention:
– Cardiology follow-up for optimizing heart failure therapy
– Lifestyle and pharmacologic measures for secondary prevention of CAD
– (7) Patient and family education regarding shock, its complications, and the importance of follow-up care
//
# Ventricular Arrhythmia (Ventricular fibrillation, Ventricular tachycardia, Premature ventricular contractions)
– In ER, pt presented w/ palpitations, dizziness, near-syncope; EKG showed ventricular tachycardia (VT)
– Risk factors: Hx of MI, reduced EF, known CAD
– Differential diagnosis: VT, VF, PVCs, secondary to structural heart disease, electrolyte imbalance
PLAN
– Lab orders: CBC, CMP, Mg, Ca, troponin, BNP, thyroid function tests
– Imaging: Echocardiogram, CXR
– Continuous EKG monitoring
– (1) Acute management of VT:
– If stable: IV amiodarone 150 mg over 10 minutes, followed by infusion of 1 mg/min for 6 hours, then 0.5 mg/min
– If unstable: Immediate synchronized cardioversion (initial shock of 100-200 joules)
– (2) Management of VF:
– Immediate CPR and defibrillation (shock at 200-360 joules for biphasic defibrillators, 360 joules for monophasic)
– Post-resuscitation care following ACLS guidelines
– (3) Management of PVCs:
– Beta-blockers (e.g., metoprolol 25-50 mg orally QD)
– Monitor for frequent PVCs which might indicate underlying heart disease
– (4) Correction of electrolyte imbalances:
– IV Mg sulfate 1-2 g over 5-60 minutes and K repletion as needed
– (5) Additional investigations for underlying cause:
– Cardiac catheterization if ischemic heart disease suspected
– Holter monitoring for episodic arrhythmia detection
– (6) Long-term management:
– ICD placement considerations based on guidelines:
– Post-MI patients with EF ≤35% at least 40 days post-MI
– Nonischemic cardiomyopathy with EF ≤35% and NYHA class II-III symptoms
– Survivors of cardiac arrest due to VT or VF not due to a reversible cause
– Optimization of heart failure medications if reduced EF
– Lifestyle modifications including smoking cessation, alcohol moderation
– (7) Follow-up:
– Cardiology referral for further evaluation and management
– Regular monitoring of EF and cardiac function
– (8) Patient education:
– Understanding of arrhythmia, its triggers, and warning signs
– Importance of medication adherence and follow-up appointments
/=======================================================================================================================================
# Premature Ventricular Contractions (PVC) (Premature beats, Ventricular extrasystoles, Benign extrasystoles)
– In ER, pt reported palpitations, intermittent; EKG confirmed PVCs – wide QRS complexes not preceded by P waves
– Diagnostic criteria: Premature QRS complex >120 ms, compensatory pause following PVC
– Risk factors: Hx of CAD, electrolyte imbalances, stimulant use (caffeine, nicotine)
PLAN
– Lab orders: CBC, CMP, Mg, Ca, troponin, thyroid function tests, BNP
– Imaging: Echocardiogram to assess structural heart disease, CXR
– Holter monitor if frequent PVCs or symptomatic
– (1) Management of symptomatic PVCs:
– Beta-blockers (e.g., metoprolol 25-50 mg PO QD) as first-line therapy
– Calcium channel blockers (e.g., diltiazem 30-60 mg PO TID) if beta-blockers contraindicated
– Consider class I or III antiarrhythmic drugs (e.g., flecainide, amiodarone) in refractory cases
– (2) Correction of reversible causes:
– Electrolyte repletion as needed (Mg, K)
– Reduction or cessation of stimulant use
– (3) Cardiology consultation for:
– Further risk stratification if structural heart disease is present
– Potential need for ICD placement in high-risk patients
– (4) Lifestyle modifications:
– Avoidance of caffeine, alcohol, and smoking
– Stress reduction techniques
– (5) Follow-up and monitoring:
– Regular follow-up with cardiology
– Repeat EKG and Holter monitor as needed based on symptoms and initial findings
– (6) Patient education:
– Understanding of PVCs, potential causes, and when to seek medical attention
– Importance of lifestyle modification and medication adherence
The top medical problems commonly encountered in an Intensive Care Unit (ICU) are diverse, reflecting the critical nature of illnesses treated in this setting. Here are ten of the most common issues:
1. **Sepsis and Septic Shock:** A serious condition resulting from the body’s response to infection, potentially leading to systemic organ failure.
2. **Acute Respiratory Distress Syndrome (ARDS):** A severe lung condition often caused by a serious illness or injury, leading to low blood oxygen levels and respiratory failure.
3. **Cardiac Arrhythmias:** Irregular heartbeats, which can be life-threatening, such as ventricular tachycardia or atrial fibrillation with rapid ventricular response.
4. **Acute Renal Failure:** Also known as acute kidney injury, this is a sudden decline in kidney function, often due to critical illness, trauma, or infection.
5. **Gastrointestinal Bleeding:** This can be due to various causes like peptic ulcers, varices, or diverticulosis, requiring urgent management.
6. **Cardiogenic Shock:** A condition where the heart suddenly can’t pump enough blood to meet the body’s needs, often due to a severe heart attack.
7. **Stroke:** Including ischemic and hemorrhagic strokes, requiring intensive monitoring and management of brain swelling and other complications.
8. **Trauma:** Severe injuries from accidents or violence, often involving multiple organ systems.
9. **Neurological Disorders:** Such as status epilepticus (prolonged seizures), severe head injuries, and spinal cord injuries.
10. **Drug Overdose and Poisonings:** Intentional or accidental, requiring close monitoring and specific antidotes or supportive care.
Management of these conditions in the ICU involves a multidisciplinary approach, including specialized medical and nursing care, and often requires advanced life support technologies and medications.
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# Community-Acquired Pneumonia (CAP) (J18.9 – Pneumonia, unspecified organism; J13 – Pneumonia due to Streptococcus pneumoniae; J15.9 – Bacterial pneumonia, unspecified)
– Dx criteria: acute onset cough, fever, pleuritic CP, SOB, focal lung findings on auscultation, new infiltrate on CXR or CT
– Severity assessment: CURB-65 (Confusion, Uremia, RR ≥30, BP <90/60, Age ≥65), PSI (Pneumonia Severity Index) for mortality risk stratification
– Common pathogens:
– Typical: S. pneumoniae, H. influenzae, M. catarrhalis
– Atypical: Mycoplasma pneumoniae, Chlamydia pneumoniae, Legionella
– Viral: Influenza, RSV, SARS-CoV-2
– Possible complications: parapneumonic effusion, empyema, bacteremia, respiratory failure, sepsis
– Red flag findings: RR ≥30, SpO2 <92%, SBP <90, AMS, multilobar infiltrates, rapidly worsening clinical status
– Reassuring findings: stable vitals, improving w/ empiric ABx, mild radiographic involvement
PLAN
– (1) Admission criteria
– CURB-65 ≥2 or PSI Class III-V
– Hypoxia (SpO2 <92% on RA) or respiratory distress
– Hemodynamic instability
– Severe comorbidities or inability to take PO meds
– (2) Diagnostics
– CBC w/ diff, CMP, ABG if hypoxic
– Blood cx x2, sputum cx + Gram stain (if ICU or concern for MDR pathogens)
– Legionella + S. pneumo urine Ag (if severe, ICU, or Legionella risk factors)
– COVID-19, influenza PCR in respiratory season
– Procalcitonin (to aid in ABx de-escalation)
– CXR (baseline and to assess resolution at f/u if persistent s/s)
– (3) Empiric ABx (based on severity)
– Outpatient:
– Healthy, no comorbidities: Amoxicillin 1g TID OR doxycycline 100mg BID OR azithromycin 500mg x1, then 250mg QD x4d (only if local macrolide resistance <25%)
– Comorbidities (COPD, DM, CHF, EtOH use): Amoxicillin-clavulanate 875/125mg BID + azithromycin OR doxycycline
– Inpatient (non-severe, non-ICU):
– Ceftriaxone 1g IV Q24H + azithromycin 500mg IV QD
– OR levofloxacin 750mg IV/PO QD (if β-lactam allergy)
– ICU/severe CAP:
– Ceftriaxone 1g IV Q24H + azithromycin 500mg IV QD
– OR ceftriaxone + levofloxacin 750mg IV QD
– Add vancomycin (trough goal 15-20) OR linezolid 600mg IV Q12H if concern for MRSA
– Add piperacillin-tazobactam 4.5g IV Q6H if concern for Pseudomonas
– (4) Supportive care
– O2 therapy for SpO2 <92%
– IV fluids for hypovolemia
– Antipyretics (acetaminophen 650mg PO Q6H PRN fever)
– Cough suppressants (benzonatate 100mg TID PRN)
– DVT ppx if admitted (enoxaparin 40mg SC QD or heparin 5000U SC Q8H)
– (5) ABx duration
– Minimum 5 days, extend if severe or slow clinical response
– Criteria to stop: afebrile x48h, clinically stable, improving O2 status
– (6) Follow-up
– Outpatient: PCP f/u in 1 wk, repeat CXR in 6 wks if persistent cough or risk of malignancy (smoker >50yo)
– Inpatient: reassess in 48h for ABx de-escalation, transition to PO ABx once stable
==========================================================================================
# Community Acquired Pneumonia (J18.9 Pneumonia, unspecified organism, J18.1 Lobar pneumonia, unspecified organism, J15.9 Bacterial pneumonia, unspecified)
– Presentation: Pt in ER w/ cough, fever, SOB. Phys exam: tachypnea, decreased breath sounds, crackles. Hx of similar symptoms in past.
– Dx criteria: Clinical presentation (cough, fever, dyspnea), CXR showing infiltrates, elevated WBC.
– CXR: infiltrates consistent w/ pneumonia. Labs: elevated WBC, potential hypoxemia on ABG.
– Ddx: viral pneumonia, bacterial pneumonia, atypical pneumonia, COPD exacerbation, CHF.
– Complications: sepsis, respiratory failure, pleural effusion, empyema.
– Red flags: persistent hypoxemia, respiratory distress, hemodynamic instability.
– Reassuring findings: stable vitals, improving oxygenation, responding to Rx.
PLAN
– Labs: CBC, sputum culture, blood cultures, ABG, serum electrolytes (sNa, sK), renal function (sCr). Consider procalcitonin to guide ABx use.
– Imaging: CXR initially, consider CT if complicated or alternative diagnosis suspected.
– ABx therapy:
– Empiric ABx based on severity and risk factors. Community: Amoxicillin-clavulanate 875/125 mg PO BID or Doxycycline 100 mg PO BID for 5-7 days.
– Hospitalized, non-ICU: Ceftriaxone 1g IV QD plus Azithromycin 500mg IV QD for 5-7 days.
– ICU: Piperacillin-tazobactam 4.5g IV Q6H or Cefepime 1g IV Q8H plus Azithromycin for 7-10 days.
– Oxygen support: Supplemental O2 to maintain SpO2 >92%. Consider NIV if indicated.
– Fluid management: Balanced crystalloids, monitor for volume overload, especially in CHF, renal impairment.
– Monitoring:
– Vitals Q4H, respiratory status closely. Repeat CXR in 48-72 hrs or if worsening.
– Lab re-draws for WBC, electrolytes Q24H or PRN.
– Complication management:
– Sepsis: Broad-spectrum ABx, fluid resuscitation, vasopressors if necessary.
– Respiratory failure: Consider intubation and mechanical ventilation.
– Pleural effusion: Thoracentesis if large or symptomatic.
– Consideration for comorbidities:
– Adjust fluid management for CHF, renal impairment.
– Monitor for drug interactions in polypharmacy.
– Follow-up and transition:
– Reassess need for continued hospitalization based on clinical improvement.
– Transition to oral ABx when stable for discharge.
– Follow-up in 2-4 weeks to ensure resolution.
//
# Empty Sella Syndrome (ESS) (Diagnosis: 253.8, Secondary Empty Sella Syndrome, Idiopathic Intracranial Hypertension)
– Patient presents w/ headache, visual disturbances (bitemporal hemianopia), and hormonal deficiencies
– Phys exam: Potential signs of pituitary hormone deficiencies (e.g., hypothyroidism, adrenal insufficiency, hypogonadism)
– Imaging: MRI brain showing empty sella, pituitary gland flattened at bottom of sella turcica
– Hormonal assessment: sNa, sK, sCr, TSH, FT4, ACTH, cortisol AM levels, LH, FSH, estradiol/testosterone levels
– Secondary ESS: Consider ddx of idiopathic intracranial hypertension, chronic intracranial hypotension, prior surgery/radiation to sellar region, pituitary apoplexy
PLAN
– Diagnostic evaluation:
– MRI brain w/ and w/o contrast for pituitary and sellar assessment
– Hormonal panel: TSH, FT4, ACTH, cortisol AM levels, LH, FSH, estradiol/testosterone, prolactin, GH, IGF-1
– Hormonal replacement therapy as needed:
– Thyroxine for hypothyroidism (e.g., levothyroxine 50-150 mcg PO QD)
– Hydrocortisone for adrenal insufficiency (e.g., 10-20 mg PO QD in divided doses)
– Testosterone replacement in men if indicated (e.g., gel, patch, IM injections Q2-4wks)
– Estrogen/progesterone replacement in premenopausal women if indicated
– Regular follow-ups for hormonal levels and MRI surveillance
– In case of idiopathic intracranial hypertension:
– Weight loss counseling if BMI >25
– Acetazolamide 250-500 mg PO BID-TID
– Serial lumbar punctures if refractory to medical management
– Patient education on recognizing s/s of hormonal imbalances
– Endocrinology follow-up for long-term management and surveillance
– If secondary ESS due to prior surgery/radiation, neurosurgery/neuro-oncology consult for potential interventions
– Regular ophthalmology follow-ups if visual disturbances present
Complications and Considerations:
– Risk of chronic hormonal deficiencies requiring lifelong replacement therapy
– Potential for worsening vision loss if not adequately managed
– Need for multidisciplinary approach in secondary ESS
– Consideration of other comorbidities (e.g., obesity, hypertension) in management planning
– Monitoring for signs of increased intracranial pressure or pituitary apoplexy in acute cases
– Coordination with primary care physician for general health maintenance and screening
//
# Hospital Acquired Pneumonia (Hospital acquired pneumonia – J18.9, Ventilator-associated pneumonia – J95.851, Pneumonia due to Pseudomonas – J15.1)
– Pt hospitalized for 5 days post-surgery, developed fever, productive cough, and increasing O2 requirements
– Diagnostic criteria: New onset of respiratory symptoms after 48 hours of hospital admission, new or progressive infiltrates on chest X-ray, elevated WBC count
– Scoring systems: CURB-65 for pneumonia severity, PSI (Pneumonia Severity Index)
PLAN
– Labs and Imaging:
– CBC with differential, blood cultures, sputum culture and sensitivity, procalcitonin
– Chest X-ray to confirm diagnosis and assess extent
– Consider bronchoscopy if sputum samples inadequate or patient immunocompromised
– Antibiotic Therapy:
– Empiric broad-spectrum antibiotics initially, then tailor based on culture results
– Consider MRSA coverage (vancomycin or linezolid) and Pseudomonas coverage (piperacillin-tazobactam or cefepime)
– Duration of therapy typically 7-10 days, adjust based on clinical response and culture results
– Respiratory Support:
– O2 supplementation to maintain SpO2 >92%
– Non-invasive ventilation or mechanical ventilation if respiratory failure develops
– Monitoring:
– Daily chest X-rays to monitor progression
– Monitor vital signs, oxygen saturation, respiratory rate, and lung sounds
– Reassess antibiotic therapy based on culture results and clinical response
– Supportive Care:
– IV fluids as needed for hydration
– Antipyretics for fever (e.g., acetaminophen)
– DVT prophylaxis with low molecular weight heparin
– Nutritional support as needed
– Patient Education and Follow-up:
– Educate patient and family about HAP, its treatment, and prevention
– Smoking cessation advice if relevant
– Arrange follow-up after discharge, including chest X-ray and clinical review
//
# Pulmonary Embolism (PE) (Diagnosis: I26.9, Pulmonary Embolism without Acute Cor Pulmonale, I26.99, Chronic Thromboembolic Pulmonary Hypertension)
– PE: In ER, patient presents w/ acute SOB, chest pain, tachypnea, tachycardia; Hx of immobility, surgery, or known DVT
– Risk factors: provoking factors (surgery, trauma, pregnancy), inherited thrombophilia, cancer, OCP use
– Provoked vs Unprovoked PE: Provoked PE associated w/ transient risk factor (surgery, immobilization); unprovoked lacks identifiable risk factor, higher risk of recurrence
– Phys exam: possible signs of DVT (leg swelling, pain), signs of RV strain
– Diagnostic criteria: Wells Score or Geneva Score for pre-test probability, confirmed by imaging (CTPA or V/Q scan)
PLAN
– Anticoagulation Therapy:
– Provoked PE: UH IV or enoxaparin SC (1 mg/kg BID or 1.5 mg/kg QD) x 5-10 days, then DOAC (e.g., apixaban 5 mg PO BID for 6 months)
– Unprovoked PE: Initial UH/enoxaparin as above, then extended therapy w/ DOAC (e.g., rivaroxaban 20 mg PO QD) or VKA (INR 2-3)
– Cancer-associated PE: LMWH preferred (e.g., enoxaparin) for at least 3-6 months
– Renal impairment (CrCl <30 mL/min): UH or adjusted dose LMWH; avoid DOACs
– Diagnostic Evaluation:
– Initial labs: CBC, BMP, coagulation profile, D-dimer
– Imaging: CTPA or V/Q scan for diagnosis, doppler US for DVT
– EKG, CXR to rule out differential diagnoses (MI, aortic dissection)
– Supportive Care:
– Oxygen therapy PRN for hypoxemia
– Analgesia for chest pain
– Monitoring:
– Assess for bleeding complications, especially first 10 days
– Regular follow-up for INR if on VKA
– Duration of Anticoagulation:
– Provoked PE: 3 months
– Unprovoked PE or recurrent: Indefinite, with periodic risk-benefit assessment
– Reassess need for extended anticoagulation at regular intervals
Complications and Considerations:
– Risk of recurrent VTE, especially in unprovoked PE
– Post-PE syndrome w/ dyspnea, decreased exercise tolerance
– Chronic thromboembolic pulmonary hypertension
– Bleeding risk w/ anticoagulation, especially in elderly, renal impairment
– Interactions of anticoagulants w/ other medications
– Patient education on signs of bleeding, compliance w/ anticoagulation
– Consideration for thrombophilia workup in unprovoked PE or strong family Hx of VTE
– In pregnant patients, LMWH preferred due to safety profile
//
# Pulmonary Embolus
# Other pulmonary embolism without acute cor pulmonale (I26.99)
# Septic pulmonary embolism with acute cor pulmonale (I26.01)
# Saddle embolus of pulmonary artery without acute cor pulmonale (I26.93)
– Diagnostic Criteria: Diagnosed via CT angiography showing filling defect in pulmonary arteries; V/Q scan with high probability; evidence of DVT via duplex US; elevated D-dimer
– Potential Complications: Hemodynamic instability, RV dysfunction, recurrent emboli, pulmonary infarction
– Red-Flag Symptoms/Findings: Severe dyspnea, syncope, hypotension, RV strain on EKG (e.g., S1Q3T3 pattern), elevated troponin or BNP; reassuring findings include normal EKG and normal cardiac biomarkers
– DDx: acute coronary syndrome (ACS): MI, unstable angina, aortic dissection, pericarditis or pericardial tamponade, pneumonia, pneumothorax, COPD exacerbation, asthma exacerbation, heart failure exacerbation, costochondritis, musculoskeletal pain, anxiety/panic attack
– Basic Risk Stratification
– High Risk PE (Massive): Hypotension (SBP <90mmHg), marked RV strain
– Intermediate Risk PE (Submassive): RV strain w/o hypotension, biomarker elevation (troponin, BNP)
– Low Risk PE (Non-Massive): Absence of RV strain, hypotension, normal biomarkers
– Risk Stratification (algorithms)
– Wells Score for PE: Evaluates clinical signs, heart rate, immobility/surgery in past 4 weeks, previous DVT/PE, hemoptysis, malignancy
– Geneva Score: Considers age, heart rate, immobilization/surgery, signs of DVT, previous DVT/PE, hemoptysis, pain on deep vein palpation
– sPESI: Simplified version of PESI for quick assessment
– PESI (Pulmonary Embolism Severity Index): Assesses risk of mortality based on various clinical parameters
– Diagnostic Evaluation (detailed considerations)
– D-dimer: Rules out PE in low-risk patients (age-adjusted cutoff: age x 10 if >50 years)
– CTPA: Primary diagnostic tool (PIOPED II criteria for interpretation)
– V/Q Scan: Alternative for patients with contraindications to CTPA
– Echocardiogram: Identifies RV dysfunction, McConnell’s sign
– EKG: Sinus tachycardia, S1Q3T3, RBBB, signs of RV strain
– Additional markers: Hypoxemia (ABG), A-a gradient, respiratory alkalosis
PLAN/MANAGEMENT
– Diagnostics:
– D-dimer, troponin, BNP, ABG
– CT angiography chest
– consider EKG
– doppler US of lower extremities (r/o DVT)
– Anticoagulation (acute):
– Initiate heparin IV bolus 80 U/kg followed by continuous infusion 18 U/kg/hr, adjust based on PTT (goal 60-80 sec or 1.5-2.5 times control)
– Transition to
– warfarin PO with overlap until INR 2-3
– rivaroxaban (DOAC) 15 mg BID for 21 days, then 20 mg QD
– apixaban 10 mg BID for 7 days, then 5 mg BID
– Anticoagulation (subacute/chronic):
– Indications for long-term or life-long anticoagulation:
– Unprovoked PE (no identifiable risk factors)
– Recurrent VTE (venous thromboembolism)
– Ongoing risk factors (e.g., active cancer, genetic thrombophilia)
– Chronic thromboembolic pulmonary hypertension (CTEPH)
– Incomplete resolution of PE on follow-up imaging
– Long-term anticoagulation options:
– Rivaroxaban (DOAC): 20 mg QD
– Apixaban: 5 mg BID
– Warfarin: Maintain INR 2-3 with monthly INR monitoring
– Consider low-dose DOACs (e.g., rivaroxaban 10 mg QD after initial therapy period) for patients with higher bleeding risk
– Thrombolysis (for massive PE with hemodynamic instability):
– Alteplase 100 mg IV over 2h
– IVC filter (consider if contraindication to anticoagulation or recurrent emboli despite adequate anticoagulation)
– Supportive Care:
– Oxygen to maintain SpO2 > 90%
– IV fluids for hypotension (NS 500-1000 mL bolus, reassess)
– Vasopressors (norepinephrine) if persistent hypotension despite fluids
– Monitoring (acute):
– Continuous cardiac monitoring
– Serial EKGs
– BMP, CBC, and coagulation panel daily
– Repeat ABG as needed
– Monitoring (chronic):
– CBC, BMP, PT/INR daily while on heparin; once stable, INR monitoring every 1-2 weeks, then monthly for warfarin
– Monitor signs of bleeding (e.g., hematuria, melena, epistaxis)
– D-dimer and follow-up imaging in 3-6 months to assess for resolution or recurrence
==============================================================================================================
# Pulmonary Embolism (PE) (Diagnosis: I26.9, Pulmonary embolism without acute cor pulmonale; I26.02, Septic pulmonary embolism with acute cor pulmonale; I26.99, Other pulmonary embolism without acute cor pulmonale)
– PE: In ER, pt presents w/ acute SOB, chest pain, tachycardia. Hx of immobility, recent surgery, known DVT. Differentiate provoked vs unprovoked PE
PLAN
– Anticoagulation Therapy:
– Choice based on risk factors, patient profile:
– Cancer: LMWH (e.g., enoxaparin)
– APLAS: Warfarin
– Others: DOAC preferred over warfarin; UH for rapid reversal need
– Duration: 3 months if provoked, indefinite if unprovoked and low bleeding risk
– Reassessment of D-dimer post-treatment for decision on duration
– Thrombolytic Therapy:
– Indications: High Risk PE with hemodynamic instability
– Contraindications: Recent surgery, bleeding risk
– Agents: Alteplase (rt-PA) 100mg IV over 2h
– IVC Filter:
– Indications: Contraindication to anticoagulation, recurrent PE despite anticoagulation
– Retrieval plan essential due to complications with prolonged use
– Supportive Care:
– Oxygen therapy for hypoxemia
– Fluid management, avoiding fluid overload
– Long-term Management:
– Regular follow-up with echocardiography for RV function
– Monitoring for CTEPH development
– Lifestyle modifications, DVT prophylaxis
– Cancer screening in unprovoked PE
Complications and Considerations:
– Chronic management: Regular assessment for CTEPH
– Differential diagnosis for elevated D-dimer includes arterial thrombi, DIC, infection, renal disease
– Recurrent VTE risk assessment post-treatment
– Coordination with multidisciplinary team for comprehensive care
==============================================================================================================
# Pulmonary Embolism (PE) (Diagnosis: I26.99, Acute Pulmonary Embolism without Acute Cor Pulmonale, Pulmonary Embolism and Infarction)
– PE: In ER, patient presented w/ sudden onset SOB, chest pain, tachycardia; Hx of recent surgery, immobility, or known DVT
– Risk factors: recent surgery, prolonged immobility, cancer, OCP use, smoking, known thrombophilia
– PE suspected based on Wells Score or Geneva Score; PERC negative in low-risk patients
– Phys exam: tachypnea, tachycardia, hypoxemia, features of DVT (calf swelling, tenderness)
PLAN
– Diagnostic evaluation:
– Initial labs: CBC, BMP, D-dimer (if low/moderate clinical probability)
– EKG: look for S1Q3T3 pattern, right heart strain
– Imaging: CTPA (CT Pulmonary Angiography) as first-line, or V/Q scan if CTPA contraindicated
– Consider lower limb compression US for DVT if PE diagnosis uncertain
– Anticoagulation therapy (start immediately if high clinical suspicion):
– LMWH (e.g., enoxaparin 1 mg/kg SC BID) or
– Direct oral anticoagulants (e.g., rivaroxaban 15 mg PO BID for 21 days, then 20 mg QD) or
– UH IV if severe renal impairment or need for rapid reversibility
– Duration of therapy typically 3-6 months; longer in recurrent PE or ongoing risk factors
– Thrombolytic therapy for massive PE w/ hemodynamic instability:
– Alteplase (tPA) 100 mg IV over 2 hours (consider risk of bleeding)
– Supportive care:
– Oxygen supplementation for hypoxemia
– IV fluids cautiously if hypotensive
– Analgesia for chest pain
– Monitoring:
– Continuous cardiac monitoring for arrhythmias
– Regular assessment for bleeding complications
– Follow-up imaging and labs (D-dimer, CBC) as needed
– Consider IVC filter in patients w/ contraindication to anticoagulation or recurrent PE despite adequate anticoagulation
Complications and Considerations:
– High risk of recurrence, especially w/ unresolved risk factors
– Risk of chronic thromboembolic pulmonary hypertension
– Interactions of anticoagulants with other medications
– Bleeding risk assessment critical before initiating anticoagulation
– Consideration for the impact of anticoagulation on comorbid conditions such as renal impairment or gastrointestinal bleeding risks
– Need for coordinated care with primary care physician and possibly a hematologist for long-term management
– In case of pregnancy, consultation with a maternal-fetal medicine specialist for anticoagulation management
=============================================
# Massive Pulmonary Embolism (PE) (Diagnosis: I26.01, Acute massive pulmonary embolism with acute cor pulmonale, Acute submassive pulmonary embolism)
– Massive PE: In ER, patient presented w/ acute SOB, chest pain, hypotension (SBP <90 mmHg or drop of ≥40 mmHg for >15 mins), syncope; Hx of recent surgery or immobilization, known DVT/PE
– Risk factors: history of thromboembolism, active cancer, prolonged immobilization, recent surgery, estrogen therapy
– Phys exam: marked tachypnea, tachycardia, hypotension, signs of RV strain, possible cyanosis
– EKG findings may include: S1Q3T3 pattern, incomplete/complete RBBB, right heart strain
– Diagnostic criteria: hemodynamic instability (hypotension, shock) with imaging evidence of large PE
PLAN
– Hemodynamic support:
– IV fluids cautiously if hypotensive, avoid fluid overload
– Vasopressors (e.g., norepinephrine) if refractory hypotension
– Immediate anticoagulation:
– Unfractionated heparin IV bolus (80 units/kg), followed by infusion (18 units/kg/hr), adjust per aPTT
– Thrombolytic therapy:
– Alteplase 100 mg IV over 2 hours unless contraindicated (risk of bleeding, recent surgery)
– Monitor for signs of bleeding; avoid invasive procedures post-thrombolysis
– Advanced therapies if thrombolysis contraindicated or unsuccessful:
– Surgical embolectomy or catheter-directed therapies in specialized centers
– Monitoring and management:
– Continuous EKG and hemodynamic monitoring
– Serial echocardiograms to evaluate RV function
– ICU admission for close monitoring
– Post-stabilization anticoagulation:
– Transition to oral anticoagulants (e.g., apixaban, rivaroxaban) post-hemodynamic stabilization for 3-6 months or longer based on risk assessment
– Follow-up and prevention:
– Serial imaging to monitor clot resolution
– DVT prophylaxis and risk factor modification
– Consider IVC filter if recurrent PE despite adequate anticoagulation or if anticoagulation contraindicated
Complications and Considerations:
– Risk of chronic thromboembolic pulmonary hypertension (CTEPH)
– Post-PE syndrome with chronic dyspnea and decreased quality of life
– Bleeding complications, especially post-thrombolysis
– Right ventricular dysfunction and failure
– Recurrent venous thromboembolism
– Coordinated care with cardiology, pulmonology, and possibly hematology
– Impact on comorbid conditions like heart failure, COPD, renal impairment
– Psychological support for anxiety, PTSD-like symptoms post-PE
# Pulmonary Embolism (PE) (Diagnosis: I26.9, Pulmonary Embolism without Acute Cor Pulmonale, I26.99, Chronic Thromboembolic Pulmonary Hypertension)
– PE: In ER, patient presents w/ acute SOB, chest pain, tachypnea, tachycardia; Hx of immobility, surgery, or known DVT
– Risk factors: provoking factors (surgery, trauma, pregnancy), inherited thrombophilia, cancer, OCP use
– Provoked vs Unprovoked PE: Provoked PE associated w/ transient risk factor (surgery, immobilization); unprovoked lacks identifiable risk factor, higher risk of recurrence
– Phys exam: possible signs of DVT (leg swelling, pain), signs of RV strain
– Diagnostic criteria: Wells Score or Geneva Score for pre-test probability, confirmed by imaging (CTPA or V/Q scan)
PLAN
– Anticoagulation Therapy:
– Provoked PE: UH IV or enoxaparin SC (1 mg/kg BID or 1.5 mg/kg QD) x 5-10 days, then DOAC (e.g., apixaban 5 mg PO BID for 6 months)
– Unprovoked PE: Initial UH/enoxaparin as above, then extended therapy w/ DOAC (e.g., rivaroxaban 20 mg PO QD) or VKA (INR 2-3)
– Cancer-associated PE: LMWH preferred (e.g., enoxaparin) for at least 3-6 months
– Renal impairment (CrCl <30 mL/min): UH or adjusted dose LMWH; avoid DOACs
– Diagnostic Evaluation:
– Initial labs: CBC, BMP, coagulation profile, D-dimer
– Imaging: CTPA or V/Q scan for diagnosis, doppler US for DVT
– EKG, CXR to rule out differential diagnoses (MI, aortic dissection)
– Supportive Care:
– Oxygen therapy PRN for hypoxemia
– Analgesia for chest pain
– Monitoring:
– Assess for bleeding complications, especially first 10 days
– Regular follow-up for INR if on VKA
– Duration of Anticoagulation:
– Provoked PE: 3 months
– Unprovoked PE or recurrent: Indefinite, with periodic risk-benefit assessment
– Reassess need for extended anticoagulation at regular intervals
Complications and Considerations:
– Risk of recurrent VTE, especially in unprovoked PE
– Post-PE syndrome w/ dyspnea, decreased exercise tolerance
– Chronic thromboembolic pulmonary hypertension
– Bleeding risk w/ anticoagulation, especially in elderly, renal impairment
– Interactions of anticoagulants w/ other medications
– Patient education on signs of bleeding, compliance w/ anticoagulation
– Consideration for thrombophilia workup in unprovoked PE or strong family Hx of VTE
– In pregnant patients, LMWH preferred due to safety profile
==============================================================================================================
# Refeeding Syndrome (Diagnosis: E44.0, Moderate malnutrition; E46, Unspecified malnutrition; T73.0, Effects of starvation)
– Refeeding Syndrome: Patient w/ history of prolonged fasting, malnutrition, or recent severe weight loss. On initiation of feeding (enteral or parenteral), developed clinical features including electrolyte imbalances (hypophosphatemia, hypokalemia, hypomagnesemia), fluid shifts, and possible glucose intolerance.
– Risk factors: Chronic alcoholism, anorexia nervosa, cancer, post-surgery, chronic undernutrition
– Clinical signs: Edema, altered mental status (AMS), respiratory distress, cardiac complications
PLAN
-Initial Management
– Hold nutritional replenishment temporarily
– Monitor vitals and electrolytes closely (Q4H initially)
– IV Thiamine: 100 mg daily before and during the first week of feeding
– Multivitamin supplement: 1 tab PO QD
– Correct electrolyte imbalances:
– Phosphate: Potassium phosphate or sodium phosphate IV, dose adjusted based on levels
– Potassium: Potassium chloride (KCl) IV/PO, dose adjusted based on serum potassium
– Magnesium: Magnesium sulfate IV/PO, dose adjusted based on serum magnesium
– Initiate cautious feeding:
– Start at ≤20 kcal/kg/day (or 500 kcal/day), then gradually increase
– Monitor fluid balance and avoid aggressive fluid repletion
– Electrolyte Monitoring and Repletion:
– Serum electrolytes (including phosphate, potassium, magnesium) Q6H initially
– Adjust supplementation doses based on repeated labs
– Blood Glucose Monitoring
– Monitor glucose Q4-6H, manage glucose intolerance if present
– Continuous cardiac monitoring for first 48-72 hours
– Nutritional Support
– Nutritionist consult
– Gradual caloric escalation over days to a week
– Monitor for signs of overfeeding
– Long-term ManagementW
– Educate patient and caregivers about gradual nutritional replenishment
– Regular follow-up for nutritional status assessment
– Counseling and support for underlying conditions (e.g., eating disorders, alcoholism)
Complications to Monitor:
– Cardiac failure due to fluid shifts
– Wernicke’s encephalopathy (prevent with thiamine)
– Respiratory distress from fluid overload
– Arrhythmias due to electrolyte imbalances
– Neurostorming: In ER, patient w/ hx of severe traumatic brain injury (TBI) or post-anoxic brain injury, manifesting w/ episodes of tachycardia, hypertension, hyperthermia, diaphoresis, posturing
– Key features: Autonomic dysregulation w/ episodic, rapid onset of symptoms; may be triggered by external stimuli or spontaneously
– Risk factors: Severe TBI, anoxia, brainstem involvement
– Phys exam findings: Tachycardia, hypertension, diaphoresis, muscle rigidity, posturing, possible AMS
Complications:
– Secondary brain injury due to increased ICP and cerebral edema
– Cardiac stress, risk of arrhythmias
– Respiratory compromise
– Musculoskeletal injury due to rigidity and posturing
– Increased metabolic demand
PLAN
– Initial lab orders: CBC, BMP, LFTs, CK, serum osmolarity, ABG
– Additional lab orders: TSH, cortisol levels, troponins, EKG, EEG, brain imaging (CT/MRI) as indicated
– (1) Autonomic stabilization:
– Beta-blocker (e.g., propranolol 10-40mg PO Q6H)
– Alpha-2 agonist (e.g., clonidine 0.1-0.3mg PO Q8H)
– (2) Sedation and muscle relaxation:
– Benzodiazepines (e.g., lorazepam 1-2mg IV/PO Q4-6H PRN)
– Baclofen for muscle spasticity (10-20mg PO TID)
– (3) Temperature regulation:
– Acetaminophen 650mg PO Q4H
– Cooling measures if hyperthermia present (e.g., cooling blankets)
– (4) Neuroprotection:
– Elevate head of bed 30 degrees
– Monitor ICP if available and maintain CPP within target range
– (5) Symptom-triggered management:
– Adjust medications based on symptomatology and severity
– Close monitoring for triggers of episodes
– (6) Regular re-assessment and modification of plan:
– Neurological exams Q4H
– Vital signs monitoring Q2H
– Lab re-draws QD or as clinically indicated
– (7) Consider multidisciplinary approach including neurology, rehabilitation, physiatry
# DRESS Syndrome (L27.2 Drug Rash with Eosinophilia and Systemic Symptoms, T88.7 Unspecified adverse effect of drug or medicament, Z91.048 Other allergic condition due to drugs in personal history)
– Pt in ER w/ rash, fever, facial edema, lymphadenopathy, 2 wks post initiation of allopurinol for gout
– Key features: morbilliform rash, fever >38°C, facial swelling, lymphadenopathy, multiorgan involvement (liver, kidney)
– Past med hx includes carbamazepine use, recently stopped
– RegiSCAR criteria: Acute rash, hematologic abnormalities (eosinophilia >1.5×10^9/L, atypical lymphocytes), systemic involvement (liver, renal, lung, heart), HHV-6 reactivation
PLAN
– Immediate discontinuation of suspect drug (allopurinol, consider carbamazepine)
– Lab orders: CBC w/ diff, LFTs, renal function, serum creatinine, urinalysis, skin biopsy if needed
– Further workup for organ involvement: liver ultrasound, chest X-ray, ECG
– (1) Corticosteroid therapy:
– Prednisone 1-2 mg/kg/day PO (max 60 mg/day), taper over 6-8 wks
– IV methylprednisolone 1-2 mg/kg/day in severe cases (organ involvement)
– (2) Supportive care:
– Antihistamines for pruritus (Diphenhydramine 25-50 mg PO Q6H PRN)
– Aggressive hydration and fever management
– (3) Monitoring:
– Daily CBC, LFTs, renal function until stable
– Weekly outpatient follow-up for 1st month, then biweekly
– (4) Specialist referral:
– Dermatology for skin management
– Gastroenterology/hepatology or nephrology if organ involvement
– (5) Patient education:
– Avoidance of suspect and structurally similar drugs
– Recognition of worsening symptoms, esp. organ involvement
– (6) Consider IVIG in refractory cases or significant organ involvement
– (7) Long-term follow-up for potential sequelae and drug allergies
Mucus membranes – SJS
=============================================
# COPD Exacerbation (J44.1, J44.9, J44.0)
– COPD Exacerbation: In ER, patient presents w/ increased dyspnea, cough, change in sputum quality/quantity; hx of smoking, chronic cough, and previous exacerbations; on assessment, increased respiratory rate, use of accessory muscles, wheezing on auscultation
– Risk factors: smoking, environmental pollutants, respiratory infections, non-adherence to COPD meds
– Red-flag symptoms: cyanosis, AMS, persistent hypoxemia, hemoptysis; concerning findings: FEV1 <30%, PaCO2 >45 mmHg, PaO2 <60 mmHg on room air
– Dx criteria: Clinical diagnosis based on Hx, Phys exam; spirometry confirms COPD w/ FEV1/FVC <0.7 post-bronchodilator
– Complications: respiratory failure, pneumothorax, pulmonary hypertension
– Impact on inpatient management: influences treatment of heart failure, pneumonia, peptic ulcer disease
PLAN
– Diagnostic confirmation:
– Spirometry (if condition stable)
– CXR to rule out pneumonia, pneumothorax
– ABG/VBG for PaO2, PaCO2 assessment
– CBC, CMP, BNP if cardiac comorbidity suspected
– (1) Bronchodilator therapy:
– Albuterol nebulizer 2.5 mg Q4H
– Ipratropium bromide nebulizer 0.5 mg Q6H
– (2) Corticosteroids:
– Prednisone 40 mg PO QD for 5 days
– (3) Antibiotic therapy (if signs of bacterial infection – increased sputum purulence):
– Azithromycin 500 mg PO QD for 5 days
– Alternative: Doxycycline 100 mg PO BID for 5 days
– (4) Supplemental oxygen:
– To maintain SpO2 88-92%
– (5) Non-invasive ventilation:
– For severe exacerbations w/ respiratory acidosis (pH <7.35, PaCO2 >45 mmHg)
– (6) Deep vein thrombosis prophylaxis:
– Enoxaparin 40 mg SC QD
– (7) Smoking cessation counseling and medication adjustment:
– Bupropion or Varenicline as appropriate
– Review and optimize maintenance COPD medications
– (8) Pulmonary rehabilitation referral:
– For all patients post-exacerbation
– (9) Vaccinations:
– Influenza, pneumococcal vaccines
– (10) Follow-up:
– Spirometry in 4-6 weeks
– Follow-up with pulmonology in 1 month
– (11) Consideration of comorbidities:
– Heart failure, OSA, GERD, anxiety/depression management
DECAF Score for Acute Exacerbation of COPD
Predicts in-hospital mortality in acute COPD exacerbation.
Criteria Points
——————————————————-
Extended MRC Dyspnea Scale (eMRCD)
– Not too dyspneic to leave house (eMRCD 1–4) 0
– Too dyspneic to leave house but
independent with washing/dressing (eMRCD 5a) +1
– Too dyspneic to leave house and
unable to wash/dress (eMRCD 5b) +2
Eosinopenia
– Eosinophils <0.05×10⁹/L (Yes) +1
– Eosinophils ≥0.05×10⁹/L (No) 0
Consolidation on Chest X-ray
– Present +1
– Absent 0
Acidemia
– pH <7.30 (Yes) +1
– pH ≥7.30 (No) 0
Atrial Fibrillation
– Present on EKG at presentation and/or
history of paroxysmal afib +1
– Absent 0
=============================================
# Diabetic ketoacidosis
# T2DM
– DKA: In ER, patient found w/ with serum and urinary ketones, anion gap metabolic acidosis (AGAP >10, pH <7.3, BG 250-800, HCO3 15) with initial Potassium of 4.6; on assessment w/ AMS and physical s/s concerning for dehydration, Kussmaul respiration, acetone noticeable on breath
– precipitating cause ddx: infection vs. insulin non-adherence vs. EtOH/cocaine intoxication vs. initial presentation of DM vs. inflammation pancreatitis vs. ischemia/infarction (MI, CVA, gut) vs. iatrogenic (SGLTis, steroid, thiazide, dobutamine, atypical anti-psychotic)
– patient has lived with T1DM for 19 yrs w/o similar incident; per patient history DKA attributable to sensor (Dexcom) dysfunction as the device’s sensor had approached end of 10-day lifecycle.
– co-contribution from urticarial episode? – BG trends 490 (00:30) –> 247 (@ 04:50), 247 (@ 04:50 by POC), 188 (@ 05:30)
PLAN/CARE PROVIDED DURING HOSPITALIZATION
– lab orders: BMP, CBC/diff, UA, urine ketones, serum osm, serum betahydroxybutyrate, ABG/VBG
– additional lab orders to consider: troponin, EKG, BCx, UCx, CXR, amylase/lipase
– (1) Volume rescucitation:
– LR @ 15-20 cc/kg/hr [UNLESS CHF,ESRD, hypoxemia]
– Addition of D5LR @ 250mL/hr since 06:00 (for BG < 250)
– (2) Potassium repletion
– goal of 3.3 – 5.3
– Q4hr BMP
– If K w/in 3.3 – 5.3 range, Provided 20mEQ KCLs
– LOW K<3.3 Give 20-40 mEq KCl IV per hour + hold insulin!
– MOD K 3.3<K<5.3 Add 20 mEq K to IVF
– HIGH K>5.3 cont to monitor
– Continue to monitor Q2hrs initially
– (3) Insulin management:
– Initial insulin bolus (usually 6-8U)
– Insulin Infusion at 0.1 U/kg/hr with titration per unit policy
– (4) Severely low pH < 6.9 give 2 amps HCO3 dissolved in 400mML steroile water w/ 20mEq KCL over 2h
-Transition back to insulin pump (turn off for now) once anion gap is closed and patient able to tolerate PO intake
– Dietary and electrolyte management considerations per above
– Considerations for transitioning to SQ Insulin: Start if BG < 200 and pt is able to eat and two of the following are met: AG<12, HCO3>15, pH>7.3.
Start basal regimen w/ either: home glargine dose OR glargine (Lantus) at 0.25-0.4 U/kg/d OR glargine at (# units on IV gtt over past 6h x 4 x 0.7).
Start bolus regimen w/ either: 0.25-0.4 U/kg/d divided (if T1DM or unknown) OR ISS only (if T2DM).
Overlap IV/SQ insulin by 2-4h.
# Electrolyte management in the setting of DKA
# Hypomagnesemia
# Potassium management (per above)
# Phosphorus repletion guidelines
– Total body defecit but serum phos w// drop w/ insulin, only replete if <1./0 to rpevent cardiac dysfxn
– LR w/ 20 mEq/L KCL @ 250
– Once glucose <200 change to d5LR @250ml/hr
– Potassium goal of 3.3-5.3
– q2hr BMP/mg/phos – replenish PRN
# HHS
– similar to above but w/ glucose > 600mg/dl (frequently >1000), sOsm >320, pH >7.3 w/ absent or minimal ketones
– more aggressive IVF w/ 8-10L defecit (as opposed to 5-8L expected in DKA)
– Presentation: AMS (25-50%), seizures, focal neuro, volume depletion, after days-weeks of evolution (versus hours-days in DKA)
– Diagnosis: Glucose > 600 mg/dL (frequently >1000), osmolality > 320 mOsm/kg, pH > 7.3, absent or minimal ketones
– Treatment: As above for DKA w/ modifications: more aggressive IVF (~8-10 L deficit); goal glucose 250-300 mg/dL (in DKA, 150-200); transition to SQ insulin when BG<300 and mental status improved and patient is able to eat
=============================================
=============================================
# Persistent Air Leak after Chest Tube Placement (Pneumothorax, Iatrogenic Pneumothorax, Traumatic Pneumothorax)
– Persistent air leak: noted post chest tube placement for pneumothorax, lasting >5-7 days
– Diagnostic criteria: Continuous bubbling in water seal chamber of chest tube system, no resolution on CXR
– Assess for: size & location of pneumothorax, chest tube position & function, underlying lung pathology (COPD, bullae)
– Risk factors: High positive ventilation pressures, COPD, lung infection, pleural adhesions, previous thoracic surgeries
– Scoring systems: Light’s criteria for pleural effusion (if applicable), CURB-65 for pneumonia risk (if infection suspected)
– Review recent imaging: CXR, CT chest (for underlying pathology, tube position, leak evaluation)
– Assess patient’s symptoms: dyspnea, pain, cough, sputum production
PLAN
– (1) Air leak management:
– Chest tube patency check
– Optimize chest tube suction (start w/ -20 cm H2O, adjust per clinical response)
– Consider water seal if small leak & stable pneumothorax size
– (2) Pleural pressure management:
– Evaluate for pleurodesis candidacy (chemical or mechanical)
– Thoracic surgery consult for persistent large leaks or failed pleurodesis
– (3) Symptom control:
– Analgesia: Acetaminophen 1g PO Q6hrs or Ibuprofen 400mg PO Q6hrs
– Consider thoracic epidural for severe pain
– (4) Monitoring:
– Daily CXR for pneumothorax size, chest tube position
– Repeat chest CT if no improvement or worsening symptoms
– (5) Additional diagnostics if indicated:
– Bronchoscopy for persistent large air leaks
– Repeat pleural fluid analysis if effusion present
– (6) Considerations for discharge planning:
– Pleurodesis success assessment
– Home oxygen therapy if persistent hypoxemia
– Pulmonary rehabilitation referral for COPD patients
# Oliguria (Oliguria, R34; Acute kidney failure, N17.9; Chronic kidney disease, N18.9)
– Defined as urine output <0.5 mL/kg/hr for >6 hrs in adults or <1 mL/kg/hr in children
– Etiologic considerations:
– Prerenal: hypovolemia (hemorrhage, dehydration, over-diuresis), low cardiac output (CHF, cardiogenic shock), systemic vasodilation (sepsis, cirrhosis)
– Intrinsic renal: ATN (ischemic vs. nephrotoxic), glomerulonephritis, interstitial nephritis, vascular causes (HUS/TTP, atheroembolic disease)
– Postrenal: bilateral urinary tract obstruction (BPH, nephrolithiasis, malignancy, neurogenic bladder)
– Risk stratification: AKI staging (KDIGO criteria)
– Stage 1: sCr increase 1.5-1.9x baseline OR urine output <0.5 mL/kg/hr x6-12 hrs
– Stage 2: sCr increase 2.0-2.9x baseline OR urine output <0.5 mL/kg/hr x>12 hrs
– Stage 3: sCr increase ≥3.0x baseline OR urine output <0.3 mL/kg/hr x>24 hrs OR anuria x12 hrs
## PLAN
– Initial diagnostics:
– Labs: CBC, CMP (sCr, BUN, K, Phos, Ca), ABG/VBG (metabolic acidosis), LDH, haptoglobin (if hemolysis suspected)
– UA w/ microscopy:
– Prerenal: benign, hyaline casts
– ATN: muddy brown granular casts, epithelial casts
– AIN: WBC casts, eosinophils, hematuria
– GN: RBC casts, proteinuria
– Postrenal: bland sediment
– Urine studies: urine Na, urine Cr, FeNa (prerenal <1%, ATN >2%)
– Imaging:
– Bladder scan (r/o urinary retention)
– Renal US (hydronephrosis in postrenal, small echogenic kidneys in CKD)
– Management by Etiology:
– Prerenal:
– Fluid resuscitation (NS or LR bolus 1-2L, then reassess UOP)
– Hold nephrotoxic agents (NSAIDs, ACEi/ARB, aminoglycosides)
– If CHF/cirrhosis: judicious volume replacement, diuretics if fluid overloaded
– Intrinsic renal:
– ATN: Supportive care, avoid nephrotoxins, optimize perfusion
– GN: Consider steroids, immunosuppressants if indicated (r/o RPGN, nephrology consult)
– AIN: Discontinue offending agent (ABx, PPI, NSAIDs), consider steroids if severe
– Postrenal:
– Foley catheter if bladder outlet obstruction
– Urology consult for nephrostomy/stenting if obstructive uropathy
– Dialysis indications (AEIOU):
– Acidosis (refractory metabolic acidosis)
– Electrolytes (severe hyperkalemia, K >6.5 refractory to medical tx)
– Intoxications (dialyzable toxins: lithium, methanol, ethylene glycol)
– Overload (refractory volume overload w/ pulmonary edema)
– Uremia (encephalopathy, pericarditis, bleeding)
– Monitoring:
– Hourly UOP (goal >0.5 mL/kg/hr)
– Q4-6hr BMP if AKI progressing
– Strict I/Os, daily weights
– Nephrology consult if oliguric AKI persists >48hrs or requires dialysis consideration
pulm exam goood
Pt alert, oriented x3, no resp distress. Chest insp: symm, no deformities. Palp: no tenderness, tymph to perc, no lags. Ausc: bilat vesic breath sounds, no wheezes/rhonchi/crackles. No clubbing/cyanosis/edema.
no resp distress. Chest insp: symm, no deformities. Palp: no tenderness, tympanic to perc, no lags. Ausc: bilat vesic breath sounds, no wheezes/rhonchi/crackles. No clubbing/cyanosis/edema.
# TCA overdose
– Diagnostic criteria: AMS or coma + anticholinergic toxidrome (tachycardia, dry mucosa, mydriasis, urinary retention) + EKG changes (QRS >100 ms, R wave in aVR >3 mm, right axis deviation, QTc prolongation) + possible hypotension or seizures
– Red-flag features: widened QRS >100 ms (risk of seizure), QRS >160 ms (risk of ventricular arrhythmia), R in aVR >3 mm, refractory hypotension, new-onset seizures, AMS or coma, respiratory depression, acidosis on VBG/ABG
– Complications: seizures, ventricular arrhythmias, cardiogenic shock, aspiration PNA, rhabdomyolysis, intubation w/ prolonged ICU stay
– Inpatient management considerations: sedation and anticholinergic effects may complicate glycemic control, mechanical ventilation, or weaning from sedation; cardiac instability may delay procedures or anticoagulation for other issues (e.g. DVT/PE)
– Reassuring findings: QRS <100 ms, hemodynamic stability, normal mental status, no seizure activity, pH >7.35, negative drug screen
PLAN
– lab orders: BMP, Mg, phos, ABG/VBG, lactate, serum drug tox panel (incl TCA level if available), serum EtOH, ASA, APAP, UDS, UA
– EKG: obtain on presentation and repeat Q30min x 2h or PRN until stable
– cardiac monitoring x 24h minimum, telemetry or ICU depending on severity
– (1) Gastric decontamination if <2h post-ingestion:
— activated charcoal 1g/kg PO/NGT (max 50g) once if airway protected
– (2) Sodium bicarb for cardiac membrane stabilization:
— if QRS >100 ms or R in aVR >3 mm, started IV NaHCO3 bolus 1-2 mEq/kg IVP (usually 1-2 amps) q3-5min PRN to narrow QRS
— followed w/ NaHCO3 gtt: 150 mEq NaHCO3 in 1L D5W at 150-250 mL/hr, titrated to maintain serum pH 7.45-7.55 and QRS <100 ms
— maintain goal sNa 145-155
— monitor Q1-2hr ABGs, sNa, sK
– (3) Hypotension management:
— IVF boluses 10-20 cc/kg NS or LR x 2 PRN MAP <65
— if refractory, started norepinephrine 2-10 mcg/min IV and titrated to MAP >65
– (4) Seizure prophylaxis/management:
— benzodiazepines: lorazepam 2-4mg IV Q5min PRN seizure
— avoid phenytoin (ineffective in TCA-induced seizures)
– (5) Intubation if LOC, respiratory failure, or pCO2 >50 mmHg on VBG
– (6) Temperature monitoring: Q2-4hr, actively rewarmed if <35°C (common due to CNS depression)
– (7) Consider lipid emulsion therapy for refractory cardiotoxicity: 20% lipid emulsion 1.5 mL/kg IV bolus over 1 min → gtt 0.25 mL/kg/min x 30-60min
– (8) ICU transfer if: QRS >160 ms, seizures, need for vasopressors, severe AMS, or ventilator dependence