Table of Contents

Approach to On-Call Internal Medicine Emergencies and Issues

Primer

Common Internal Medicine issues and emergencies for psychiatric patients may occur. It is important for any psychiatrist to have a good approach to these issues and to direct the right work up and medical care and not confound psychiatric symptoms with acute medical issues.

Physical Exam

Vital Signs

Never forget the vital signs because they are vital. Always remember the A-B-C-Ds:

The Unresponsive Patient

Neurologic

Altered Level of Consciousness or Delirum

Stroke

Seizures

Chest Pain

Initial
Physical Exam
Differential Diagnosis
Investigations
Management

Management of Chest Pain

Management Pearls
STEMI Call a code STEMI. Give ASA 160mg, clopidogrel 300-600mg or ticagrelor 180mg loading dose, and unfractionated heparin or low molecular weight heparin (consider bleeding risk, can choose fondaparinux). Pain can be managed with morphine. Oxygen should also be given. Less likely to be MI if the pain is reproduced on palpation
NSTEMI Can use the same medications as above for STEMI Less likely to be MI if the pain is reproduced on palpation
Pulmonary Embolism (PE) PEs are notoriously difficult to detect, but you must be aware of when it could happen! CTPE can be ordered (The risk of contrast-induced nephropathy is negligible if the patient does not have an AKI or CKD (roughly as long as Cr < 100 you are OK), else you have to think twice about it). Anticoagulation is the first-line treatment (see side-bar for more details). If the pain is pleuritic with respiration, consider a pulmonary embolism. Any new or worsening tachycardia plus hypoxia with no ECG changes should make you suspect a possible PE. In conjunction with a normal CXR, this would be enough to treat empirically with anticoagulation
GERD Should be a diagnosis of exclusion in new-onset chest pain. Treat with Almagel (magnesium hydroxide) or ranitidine

PE Patients Can Become Rapidly Unable

Any sign of hemodynamic instability should prompt involvement of a rapid response team. These patients can be quite tenuous and deteriorate quickly

PEs, Anticoagulation, and CTPEs

Here are some clinical pearls to think about in the management of PEs:
  • Anticoagulation does not necessarily need to be started right away, even if you order a CTPE. However, in a severely ill patient with significant symptoms or hemodynamic changes, (such as tachycardia, hypoxia, and normal CXR), then you should more urgently
  • Subsegmental PEs are controversial and may not account for your patient’s pain

Anticoagulation

Here are some tips for dosing depending on the type of heparin you choose:
  • Unfractionated heparin
    • The nomogram seems confusing but in essence: more heparin makes blood thinner, and less heparin makes it less thin. The nomogram provides dose guidance for this. Look for the patient’s weight on the left, and choose a loading dose based on weight if you want them anticoagulated faster. Check the PTT q6h and adjust increase or decrease the infusion rate. Generally, you want a high dose nomogram for treatment and a low dose nomogram if you are concerned about bleeding risk
  • Low-molecular weight heparin (LMWH)
    • Enoxaparin 1mg/kg SC will last for 12h
    • Tinzaparin 175u/kg SC rounded to nearest cartridge dose

The ECG In Acute MI, Stephen W. Smith, MD Fig. 1

Tachycardia

ECG Strip Reading

Is the QRS narrow or wide?
  • If wide: it is VT until proven otherwise
  • If narrow: it is either sinus tachycardia vs SVT
    • Sinus tachycardia
      • ECG shows: P before every QRS, QRS after every P, P is upright in leads I, II, PR is fixed
      • Differential diagnosis: Pain, agitation, withdrawal, sepsis, volume depletion, PE, heart failure, pain, agitation, withdrawal, sepsis, volume depletion, heart failure
    • SVT
      • Most commonly will be due to Atrial fibrillation (AF) or Atrial flutter
        • How fast is the HR?
        • Are they on rate control agents already?
        • Again, if unstable, call for help!
        • Think of why this is happening! Treat underlying cause first, rather than just increasing meds

Atrial Fibrillation

A HR <110 is acceptable. Don’t need to be aggressive unless there are ischemic symptoms (angina, troponin bump, ECG changes, etc).

Respiratory Distress

Urgent and Emergent Causes of Dyspnea or Desaturation

History and Physical Investigations
Pneumothorax Hyperresonance, poor a/e, tracheal deviation CXR (if hypotensive, aspirate immediately)
Myocardial Infarction Rapid onset, cardiac RFs, Hx CAD, chest pain ECG, serial troponin
Pulmonary Embolus Wells Criteria for PE D-dimer, CT-PA
Heart failure Hx HF, ↑ JVP, crackles, edema BNP, CXR, ECG
Severe asthma Hx asthma, wheezing Trial of B-agonist
COD exacerbation Hx COPD, wheezing CXR, ABGs, peak flow
Anaphylaxis New meds or exposures, angioedema, ↓ BP N/A
Severe anemia Pallor, tachycardia CBC, Crossmatch
Septic pneumonia Fever, tachycardia, ↓ BP CXR, blood cultures
Metabolic acidosis Ingestions, renal pt, T1DM ABG, lytes, Cr, glucose

Hypotension/Hypertension

When managing issues around blood pressure, there are only four possible scenarios:

  1. Hypotensive Bad: BP is low and the patient is dying!
  2. Hypotensive Fine: BP is low, patient is fine, should we hold antihypertensives?
  3. Hypertensive Fine: BP is high, patient is fine, do we treat with antihypertensives?
  4. Hypertensive Bad: BP is high, and patient is having associated symptoms

Hypotension

Red Flags for Acute/Critical Care Involvement

  • 4 Red Flags:
    • Always treat the patient and not the number; vitals are sensitive but not specific
    • Altered level of consciousness
    • Trend of blood pressure getting progressively lower
    • Decreasing urine output
  • Management
    • If due to sepsis, give more IV fluids and repeat lactate
    • If due to dehydration, give IV fluids (consider 0.9% NS to avoid inducing hyponatremia)[1]
    • If due to heart failure (especially if patient is hypoxic from heart failure), do not give more IV fluids

Urgent and Emergent Causes of Hypotension

History and Physical Investigations
Hypovolemia Tachycardia < 150, ↓ urine output, ↓ JVP Cr, BUN, lactate, Group&Sc, Xmatch
Anaphylaxis Exposure to agent, SOB, wheezing, angioedema Clinical Dx (act quickly), give 0.3 mg IM epinephrine
Sepsis Fever, source of infection (skin, resp, abdo, urine) CBC, U/A, CXR, U/S, blood and urine, C&S
Arrythmia/cardiogenic shock Palpitations, pulse irregular, dyspnea, ECG ECG
Cardiac tamponade Beck's triad - muffled heart sounds, ↑ JVP, hypotension ECG, CXR, Echo
Pulmonary embolus PERC, Wells criteria for PE D-dimer, CT-PA

General Management of Hypotension

Stopping Antihypertensives

Easy to Stop • Calcium channel blockers (amlodipine)
• ACE inhibitors (-prils)
• ARBS (-sartans)
• Hydrochlorothiazides
Harder to Stop • Beta blockers (generally do not cause that much hypotension and may be important in avoiding tachyarrythmias such as atrial fibrillation which may worsen heart failure)
• Furosemide (may be needed in ongoing treatment of heart failure)

Hypertension

Hypertensive Urgency vs. Emergency

Hypertensive Urgency Hypertensive Emergency/Crisis
BP SBP > 180
DBP > 120
SBP > 180
DBP > 120
Presentation • Asymptomatic or no evidence of end-organ damage
• Use PO meds to decrease by 25-30%
Outpatient management
Evidence of end organ damage: CNS (altered LOC, asterixis), cardiac, renal, papilledema.
Treatment Outpatient management. Use PO meds to decrease BP by 25-30%. Inpatient management. Use IV meds to decrease BP by 25-30%.
Medications In a patient with HTN pick hydrochlorothiazide over furosemide. But for patients with acute congestive heart failure, Lasix (furosemide) is superior to HCT Hydralazine, captopril, labetalol IV (continuous infusion), nitroglycerin patch
Example Will want to lower BP to 160/100 using PO meds Nitropatch 0.8mg + labetalol 20mg IV (0.5mg/min infusion)

When Should You Really Worry About High Blood Pressure?

  • SBP > 180 AND there are signs of end organ damage (i.e. - headache, visual change, chest pain)
    • Here you might actually treat the number and less so the patient. The only situation where you would allow the blood pressure to remain high is if it is a post-stroke patient
  • If the SBP > 180, but they are asymptomatic, don't panic
    • You have time (24 hours) to treat the high blood pressure, and in fact you may not want to treat too quickly, especially if they have been hypertensive for a long time

Treating and Managing Asymptomatic Hypertension

  • Review current medications
    • Can give an extra dose, titrate up current regimen or give AM dose early depending on clinical situation
  • Adding agents
    • Most of these will not act immediately, but again unless it is an emergency there is no need to lower urgently
    • Beta blockers are NOT good antihypertensives
    • Calcium channel blockers: amlodipine (5mg and go up in 2.5 to 5 mg increments)
    • Thiazide diuretics: hydrochlorothiazide (12.5mg and go up by 12.5mg increments)
    • ACE inhibitors: ramipril (2.5mg BID and go up by 2.5 mg increments, stop at 10 mg)
    • Vascular smooth muscle dilators: hydralazine (5mg-10mg TID and go up in 5mg increments), good in renal failure. More rapid acting, can give an extra dose if needed.

Glucose Abnormalities

Hyperglycemia

  • Hyperglycemia is usually of little significance acutely unless the patient is in diabetic ketoacidosis (DKA) or in a hyperosmolar hyperglycemic state (HHS) from it, and that usually requires at least a few day's worth of insulin deficiency before this happens.
    • Diabetic ketoacidosis (DKA) or hyperosmolar hyperglycemic state (HHS) are the most serious, acute metabolic complications of diabetes, but other differentials include dietary indiscretion and new onset or uncontrolled diabetes
      • DKA is a state of absolute insulin deficiency, hyperglycemia, anion gap acidosis, and dehydration. It classically occurs in younger patients (<65 years) with Type 1 diabetes and usually evolves rapidly over 24 hours. The most common causes are infections, disruption of insulin therapy, or as the presentation of new onset diabetes.
      • HHS is a state of hyperglycemia, hyperosmolarity, and dehydration without significant ketoacidosis. It is typically seen in Type 2 diabetics, and has a higher mortality rate compared to DKA, and occurs in older patients. It most commonly occurs in older patients (>65 years old) with infections and/or poorly controlled Type 2 diabetes and evolves over several days.
      • Both DKA and HHS originate from a reduction in insulin and an increase in counter-regulatory stress hormones.
    • The key here is that in DKA the patient will be acidotic (low bicarb, high anion gap). In the context of positive ketones and known diabetes – this is DKA regardless of the glucose value (euglycemic DKA is possible and has a much higher incidence with SGLT2 inhibitors)

Mnemonic

The 6 I's can be used to remember the I’s of DKA and HHS:
  • I - Insulin deficiency (New onset T1DM, failure to take enough insulin)
  • I - Infection is the most common precipitating factor (Pneumonia, UTI)
  • I - Ischemia or Infarction (MI, CVA, Acute Mesenteric Ischemia)
  • I - Inflammation (Pancreatitis, Cholecystitis)
  • I - Intoxication (Alcohol, Drugs)
  • I - Iatrogenesis (Glucocorticoids, Thiazides)
  • Correcting Hyperglycemia
    • You will likely be paged for blood glucose >20 because that’s how the default sliding scale orders are written
      • Consider calling the hospital pharmacist if available to help with insulin dosing as well.
      • Easy version: just give the maximum dose according to the sliding scale, or just give 2 units of insulin and ride it out
      • Most sliding scales will have insulin Lispro (fast-acting insulin)
    • Before administration of insulin, always ask:
      • When was the last meal or snacks?
      • What are the vitals?
      • Look at the blood sugar trends over past week and baseline (if available)
      • Remember that treating hyperglycemia can cause potassium shifts and may result in ECG abnormalities
    • Most individuals with hyperglycemia will in fact be asymptomatic
      • The classic symptoms that you should ask about include:
        • Polyuria
        • Polydipsia
        • Polyphagia
        • Weight loss
    • Ask about symptoms of DKA:
      • Abdominal pain
      • Hyperpneic respirations (fast and deep Kussmaul respirations)
      • Hypotension
      • Ketotic breath (fruity odor in DKA)
      • Marked tachycardia (in patients with marked acidemia or severe hyperglycemia, extracellular potassium shifts may result in ECG manifestations of hyperkalemia despite total body losses)
      • Neurologic symptoms (seizures, focal weakness, lethargy, coma, death)

General Blood Sugar Targets

  • General Blood Sugar Targets
    • Pre-prandial goal: 5-8
    • Random blood glucose: <10
    • Start correcting if the BG > 10
    • Wait about 2 hours after eating or insulin administration to check the blood glucose again

Insulin Types

Class Examples Onset Peak Duration Uses
Rapid Acting Lispro/Humalog
Aspart/Novorapid
Glulisine/Apidra
15 minutes 1 to 2 hours 4 hours “Bolus” insulin: for glucose elevations related to meals/carb intake, or to correct high BG
Short Acting Regular or Toronto (Humulin R or Novolin R) 30 minutes 2 to 4 hours 6 to 8 hours “Bolus” insulin: for glucose elevations related to meals/carb intake, or to correct high BG
*Used for insulin infusions
Intermediate Acting NPH (Humulin N or Novolin N) 1 to 2 hours 8 hours 12 to 18 hours “Basal” insulin: for glucose elevations related to hepatic glucose production in fasting state
*Peak can cover lunch
Long Acting Detemir/Levemir
Glargine (Lantus, Toujeo)
1 to 2 hours None 12 to 24> hours “Basal” insulin: for glucose elevations related to hepatic glucose production in fasting state

Hypoglycemia

Electrolyte Abnormalities

Hyperkalemia

Hypokalemia

Hypomagnesemia

Hypophosphatemia

Hypernatremia

Hyponatremia

Pain

Insomnia

Constipation

Treatment

Urinary Tract Infections

Other Lab Abnormalities

Resources