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‫انلادبع قراط‬ ‫رصانلادبع قراط‬

‫رصانلادبع قراط‬ ‫قراط دلاخ‬

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‫دمحم قورشانلادبع قراط‬ ‫حملادبع نيدلا رون‬ ‫انلادبع قراط‬

‫شه رهاس‬

‫‪Clinical Reference Guide‬‬ ‫‪Page 5 of 5‬‬

ICU & Cardiology Clinical Guidelines
Quick Reference Manual for Critical Care & Managed Therapies

Q1: Thrombosis Prophylaxis vs. Bleeding Risk Scoring

In the ICU or general medical wards, balancing clotting risk against bleeding risk is essential before starting
chemical venous thromboembolism (VTE) prophylaxis.

Thrombosis Prophylaxis Scores

• Caprini Score: Primarily used for surgical patients. It uses a detailed checklist of over 40 risk factors to
categorize patients into low, moderate, high, or highest VTE risk.
• Padua Prediction Score: Typically used for hospitalized medical patients. A score of 4 or more indicates
high VTE risk, warranting pharmacological prophylaxis (like low-molecular-weight heparin).

Bleeding Risk Scores

• HAS-BLED Score: Primarily used for patients with Atrial Fibrillation (AF) to assess bleeding risk before
starting oral anticoagulation. A score of 3 or more indicates high risk, requiring caution and regular review.
• IMPROVE Bleeding Score: Used specifically for hospitalized medical patients to assess whether the risk of
running VTE prophylaxis outweighs the benefits. A score of 7 or more suggests a high risk of major bleeding.

Q2: Stress Ulcer Prophylaxis (SUP)

Definition
Stress Ulcer Prophylaxis (SUP) is the administration of medications (typically Proton Pump Inhibitors [PPIs] or
Histamine-2 Receptor Antagonists [H2RAs]) to prevent acute gastric mucosal lesions and subsequent clinically
significant upper gastrointestinal bleeding in critically ill patients.

Risk Factors for Stress Ulcers

The risk factors are traditionally divided based on the landmark Cook criteria, which dictate when a patient must
receive SUP:

Major Risk Factors (Indication for SUP on their own)

• Mechanical ventilation expected to last greater than 48 hours.
• Coagulopathy (Platelets less than 50,000/µL, INR greater than 1.5, or aPTT greater than 2 times control).

Minor / Cumulative Risk Factors (SUP indicated if ≥ 2 are present)

• Sepsis or severe shock • Severe head or spinal cord trauma
• Acute kidney injury or RRT • History of GI bleeding within past year
• Hepatic failure • High-dose corticosteroid therapy (>250 mg
hydrocortisone equivalent daily)
• Severe burns (>35% of body surface area)

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Scoring for Stress Ulcers
While clinical practice relies directly on the presence of the major risk factors listed above, some centers use the
BALI score (incorporating Age, Mechanical Ventilation, History of Peptic Ulcer, and Renal Failure) to quantify GI
bleeding risk in the ICU.

Q3: Range of Blood Glucose Level in ICU Patients

For most critically ill or ICU patients, a moderate glucose target is preferred over tight glycemic control to prevent
dangerous hypoglycemic episodes (as proven by the NICE-SUGAR trial).

140–180 > 180 < 70

TARGET RANGE (MG/DL) INSULIN TRIGGER (MG/DL) HYPOGLYCEMIA (MG/DL)
7.8 → 10.0 mmol/L Initiate IV Infusion 3.9 → 4.0 mmol/L

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 Q4: Definition of MAIDENS
MAIDENS is a highly useful clinical mnemonic used by pharmacists and clinicians during ICU rounds to perform a
comprehensive, systematic daily medication review for critically ill patients.

Medication Reconciliation: Ensuring home meds are appropriately continued, held, or adjusted upon
M ICU admission/transfer.

Antibiotics / Antimicrobials: Checking for proper dosing, renal adjustments, cultures, and daily de-
A escalation or discontinuation opportunities.

Indications: Confirming that every single prescribed drug has a valid, current clinical indication
I (eliminating unnecessary medications).

Dosing: Verifying that doses are accurate, especially considering fluctuating renal and hepatic function
D in critical illness.

Electrolytes: Reviewing and correcting daily lab values (Potassium, Magnesium, Phosphorus, Calcium,
E Sodium) to prevent arrhythmias or weakness.

No Known Drug Allergies (NKDA) / Side Effects: Monitoring for adverse drug reactions, toxicities, or
N drug-drug interactions.

Stress Ulcer / Sedation / Sepsis: Reviewing the need for continued SUP, optimizing sedation scales
S (like RASS targets), and ensuring adherence to sepsis bundles if applicable.

Q5: Management of Hepatorenal Syndrome (HRS)

Hepatorenal syndrome is a form of functional acute kidney injury occurring in patients with advanced liver disease
or cirrhosis. The core goal of management is reversing severe splanchnic vasodilation to restore renal perfusion.

1. General Initial Steps

• Discontinue all nephrotoxic drugs (NSAIDs, aminoglycosides, contrast).
• Hold diuretics (Spironolactone, Furosemide).
• Identify and aggressively treat any precipitating factors, particularly Spontaneous Bacterial Peritonitis (SBP)
or other infections.

2. Pharmacological Volumization and Vasoconscription

The standard of care is a combination regimen:

• Albumin: Given at 1 g/kg on Day 1 (up to 100g), followed by 20 → 40 g/day. This expands intravascular volume.
• Vasoconstrictor (Pick ONE of the following options):
◦ Terlipressin: (Preferred choice) Given as an IV bolus or continuous infusion. It targets V receptors to
1
constrict splanchnic vessels.
◦ Norepinephrine: Used as a continuous IV infusion in ICU settings; highly effective at raising systemic
vascular resistance.
◦ Midodrine + Octreotide: An oral/subcutaneous alternative used primarily on general floor settings if
Terlipressin or Norepinephrine cannot be used.

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3. Definitive Treatment
• TIPS (Transjugular Intrahepatic Portosystemic Shunt): Can reduce portal hypertension in select patients
who fail medical therapy.
• Liver Transplantation: The absolute, definitive curative treatment for underlying liver failure and HRS.

Q6: Antifailure Measures (Medications) for HFrEF

The pharmacological management of Heart Failure with Reduced Ejection Fraction (LVEF ≤ 40%) revolves around
the "Four Pillars" of Guideline-Directed Medical Therapy (GDMT). These medications reduce mortality, prevent
hospitalizations, and promote cardiac remodeling.

Medication Class Core Examples Clinical Purpose

1. ARNI (Preferred) Sacubitril/Valsartan (ARNI) Neurohormonal blockade; induces vasodilation

or ACEi / ARB Lisinopril, Enalapril (ACEi) and lowers afterload.
Losartan, Valsartan (ARB) Note: Never mix an ARNI and an ACEi; requires a
36-hour washout period.

2. Beta-Blockers Carvedilol, Metoprolol Blocks chronic sympathetic overactivation. Must

Succinate, Bisoprolol use one of these three specific evidence-based
beta-blockers.

3. MRA (Mineralocorticoid Spironolactone, Eplerenone Provides aldosterone blockade to prevent cardiac

Receptor Antagonists) fibrosis and remodeling. Monitor potassium
closely.

4. SGLT2 Inhibitors Dapagliflozin, Empagliflozin Promotes osmotic diuresis and improves

myocardial energetics; drastically reduces heart
failure hospitalizations.

Symptomatic & Add-on Therapies

• Loop Diuretics (Furosemide, Bumetanide): Used strictly for congestion and fluid overload management
(symptom control); they do not provide a survival benefit on their own.
• Hydralazine + Isosorbide Dinitrate: Added for patients who cannot tolerate ARNI/ACEi/ARB due to
hyperkalemia or renal failure, or as an add-on therapy specifically proven to reduce mortality in African
American patients.
• Ivabradine: Considered if the patient is in sinus rhythm with a resting heart rate ≥ 70 bpm despite being on the
maximum tolerated dose of a beta-blocker.

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 Clinical Protocol & Medical Responses

Q 7: Scoring for Patients with Cirrhotic Liver

In clinical practice, two primary objective scoring systems are used to assess the severity, prognosis,
and mortality risk of liver cirrhosis, while a third evaluates acute complications:

• Child-Pugh Score: Classifies patients into Classes A, B, or C to assess 1-year and 2-year survival
rates. It relies on 5 parameters (3 laboratory and 2 clinical):
◦ Laboratory: Total Bilirubin, Serum Albumin, and INR (Prothrombin Time).

◦ Clinical: Degree of Ascites and Grade of Hepatic Encephalopathy.

• MELD Score (Model for End-Stage Liver Disease): A logarithmic formula calculating a score from
6 to 40, primarily used to prioritize patients for liver transplantation and predict 3-month mortality. The
standard MELD-Na score utilizes: Serum Creatinine, Total Bilirubin, INR, and Serum Sodium.

• Maddrey’s Discriminant Function (DF): Specifically calculated using Prothrombin Time and
Bilirubin to determine severity and the need for corticosteroid treatment in patients with alcoholic
hepatitis superimposed on cirrhosis.

Q 8: When to Stop IV KCl Infusion in Patients with DKA

Intravenous Potassium Chloride (KCl) replacement is critical in Diabetic Ketoacidosis (DKA)

management because insulin shifts potassium intracellularly, rapidly lowering serum levels. You should
stop or adjust the continuous IV KCl infusion when:

• Hyperkalemia develops: Serum potassium rises above 5.2 mEq/L.

• Renal compromise / Anuria: The patient stops producing urine (urine output drops below
0.5 mL/kg/hr). Potassium should never be infused in an anuric patient due to the high risk of fatal
arrhythmias.

• Transition to oral therapy: The DKA has resolved (anion gap closed, patient is alert and eating),
and the patient is safely transitioned to oral maintenance potassium if a deficit still exists.

Q 9: How to Calculate Insulin Doses?

Insulin dosing depends entirely on the clinical scenario. Below are the standard calculation frameworks
for both acute DKA management and chronic maintenance.

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1. In Acute DKA (Intravenous Regular Insulin)

• Continuous Infusion Method: Administer a fixed rate of 0.1 units/kg/hour.

• Alternative: A bolus of 0.1 units/kg followed by an infusion of 0.1 units/kg/hour.

• Adjustment Rule: If plasma glucose does not fall by 50-70 mg/dL in the first hour, verify fluid status;
if hydration is adequate, double the insulin infusion rate.

2. In Maintenance Therapy (Subcutaneous Total Daily Dose - TDD)

When initiating a basal-bolus regimen for a stable patient, calculate the Total Daily Dose (TDD):

TDD = 0.4 to 0.5 units / kg / day

Split this calculated TDD using the 50/50 Rule:

• Basal Insulin (Glargine/Detemir): Give 50% of the TDD once daily at bedtime.

• Prandial (Mealtime Rapid Insulin): Divide the remaining 50% equally among three main meals.

3. Patient-Specific Tuning Factors

• Insulin-to-Carbohydrate Ratio (ICR): Determines how many grams of carbohydrates are covered
by 1 unit of rapid-acting insulin. Calculated via the Rule of 500:

ICR = 500 / TDD

• Correction Factor / Sensitivity Factor (CF): Determines how much 1 unit of rapid insulin will drop
blood glucose (in mg/dL). Calculated via the Rule of 1800:

CF = 1800 / TDD

Q 10: Why Give Antifungal for DKA: Vfend vs. Diflucan (Fluconazole)?

Patients presenting with DKA are uniquely susceptible to highly aggressive, opportunistic fungal
infections due to the combination of low physiological pH, hyperglycemia, and elevated free iron levels in
the blood.

• The Clinical Danger: The primary fungal threat in severe, uncontrolled DKA is Mucormycosis
(Zygomycosis), followed closely by invasive aspergillosis or resistant Candida species.

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 • Why Vfend (Voriconazole) Over Diflucan (Fluconazole)?
◦ Diflucan (Fluconazole) has a narrow spectrum. It is highly effective against standard Candida
albicans but lacks activity entirely against Aspergillus species and Mucorales.

◦ Vfend (Voriconazole) is a second-generation triazole with a significantly expanded spectrum,

offering coverage against Aspergillus and fluconazole-resistant molds.

• Clinical Caveat: If Mucormycosis (rhinocerebral infection) is suspected, neither azole is the

primary choice. Direct treatment requires Liposomal Amphotericin B as the absolute gold
standard, though voriconazole or posaconazole may feature in complex polymicrobial or mold
differentials.

Q 11: Insulin Algorithm for DKA

Management follows a highly specific sequence designed to clear ketonemia while avoiding rapid shifts
in serum osmolality.

• Phase 1: Fluid Resuscitation First: Never start insulin if serum K^+ < 3.3 mEq/L. Correct potassium
first. Initiate aggressive hydration with 0.9% NaCl (1–1.5 L over the first hour).

• Phase 2: Continuous Insulin Infusion: Start Regular Insulin IV at 0.1 units/kg/hr. Target a steady
blood glucose drop of 50-70 mg/dL per hour.

• Phase 3: The Glucose Switch (Preventing Cerebral Edema): When blood glucose drops to
200-250 mg/dL, change the IV fluids to include dextrose (e.g., D5W with 0.45% NaCl). Crucial Step:
Reduce the insulin infusion rate to 0.02-0.05 units/kg/hr. Keep the insulin running to suppress
ketogenesis; use the added dextrose to prevent hypoglycemia while the anion gap closes.

• Phase 4: Resolution & Overlap: DKA is resolved when: pH > 7.3, Serum Bicarbonate ≥ 15 mEq/L,
and Anion Gap < 12 mEq/L. Transition: Administer subcutaneous basal insulin 2 hours before
shutting off the IV insulin infusion to prevent rebound ketoacidosis.

Q 12: Statin to DKA, Why?

Statins are not prescribed to treat the acute episode of DKA itself; rather, they are initiated because a
DKA presentation exposes underlying cardiovascular risks and metabolic disruptions:

• Extreme Hypertriglyceridemia: The profound insulin deficiency in DKA shuts down lipoprotein
lipase. This prevents the clearance of VLDL and chylomicrons, leading to severely elevated
triglycerides (sometimes exceeding 1000 mg/dL), which puts the patient at high risk for acute
pancreatitis. Statins help stabilize lipid profiles post-crisis.

• Cardiovascular Primary/Secondary Prevention: According to the American Diabetes Association

(ADA) guidelines, diabetes is an independent coronary risk equivalent.

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 • Age and Risk Stratification: Any patient with diabetes aged 40–75 requires a moderate-to-high
intensity statin for primary cardiovascular prevention, regardless of baseline LDL levels. A DKA
admission serves as a critical clinical touchpoint to close this gap in guideline-directed medical
therapy.

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