Introduction

There are three key ingredients to ensure accurate BP measurement at home:

• Choosing the right time.
• Mastering the right technique.
• Using the right device.

Choosing the right time.

The short answer: There’s no single perfect time—but there are best practices.

You can check your blood pressure at different times throughout the day, and I often encourage my patients to do so. However, for the most accurate reading, avoiding certain activities beforehand is crucial.

Tips for Accurate Blood Pressure Readings (Per ACC & AHA Guidelines):

✅ Avoid caffeine, alcohol, exercise, and smoking for at least 30 minutes before measuring.
✅ Sit quietly for 5 minutes before taking your reading—keep your feet flat on the floor and your back supported.
✅ Empty your bladder beforehand, as a full bladder can raise your blood pressure.

These simple steps help eliminate factors that can falsely raise your blood pressure.

What is the technique to check your blood pressure?

When it comes to accuracy, upper-arm monitors are the preferred choice. The American Heart Association (AHA) recommends arm cuff-based devices over wrist monitors because they tend to provide more reliable readings. Research has shown that upper-arm measurements align more closely with ambulatory blood pressure monitoring (ABPM)—the gold standard for assessing blood pressure.

Key Tips for Accurate Blood Pressure Readings:

✔ Use an upper-arm monitor for the most precise measurements.
✔ Keep your arm at heart level while measuring—this applies whether you’re using an upper-arm or wrist monitor.
✔ Choose the right cuff size to ensure accuracy.

Blood Pressure Cuff Sizes:

📏 Small Adult Cuff
📏 Adult Cuff
📏 Large Adult Cuff
📏 Adult Thigh Cuff

Selecting the correct cuff size is crucial—a cuff that’s too small or too large can lead to inaccurate readings. Always check the manufacturer’s sizing guide to find the best fit for your arm.

Choosing the Right Blood Pressure Cuff Size

Selecting the correct cuff size is essential for accurate blood pressure readings. The American Heart Association (AHA) recommends choosing a cuff based on your mid-arm circumference:

📏 Small Adult Cuff → 22-26 cm
📏 Adult Cuff → 27-34 cm
📏 Large Adult Cuff → 35-44 cm
📏 Adult Thigh Cuff → 45-52 cm

Why Cuff Size Matters

Using the wrong cuff size can lead to significant inaccuracies:
❌ Too small? May produce falsely high blood pressure readings.
❌ Too large? Can result in falsely low readings.

How to Ensure Accuracy

For precise measurements, choose a cuff with an inflatable bladder that spans approximately 80% of your arm circumference.

🔎 What is a cuff bladder?
It’s the inflatable chamber inside the blood pressure cuff that, when filled with air, compresses the artery to measure blood pressure accurately.

Using the right cuff improves accuracy and ensures reliable blood pressure monitoring at home.

Which Blood Pressure Monitor Should You Buy?

The American College of Cardiology (ACC) and the American Heart Association (AHA) recommend the following automated, validated blood pressure monitors for home use:

✅ Omron 10 Series BP7450 (HEM-7342T-Z)
✅ Omron Platinum BP5450 (HEM-7343T-Z)
✅ Omron M6 Comfort
✅ Withings BP-800

(I have no financial ties to these manufacturers.)

These models are known for their accuracy and ease of use, making them great choices for home blood pressure monitoring. However, even the best device won’t provide reliable results unless you follow proper measurement techniques.

Prevention

Four important practical steps to reduce the risk of acute kidney injury (AKI) in hospitalized patients:

• Adequate hydration.
• Avoiding hypotension.
• Detecting and treating urine retention early.
• Limiting the use of nephrotoxins.

Let’s break down these points a bit…

Adequate hydration

For most, adequate oral intake provides sufficient hydration. Use IV fluids only when necessary—like in cases of volume depletion or prolonged NPO status.

Precautions:

• Patients with vomiting, diarrhea, fever, or decreased oral intake for any reason have a degree of volume depletion. We must optimize their volume status with IV fluids before introducing nephrotoxic medications, even if their kidney function looks normal.
• Patients on diuretics are at higher risk of dehydration and electrolyte imbalances due to over-diuresis. I always advise my patients to stop taking diuretics if they develop vomiting, diarrhea, fever, or significantly reduced oral intake.
• Patients with rhabdomyolysis and hemolysis are at risk of developing pigment-induced nephropathy particularly when CK > 5000, aggressive IV fluid hydration should be provided to prevent that.
• Patients at risk for contrast-induced nephropathy (CIN) such as those with preexisting renal impairment, should receive IVF hydration with isotonic solutions 1 mL/kg/hour starting 6-12 hours before and continuing for 12-24 hours after the procedures.

Avoiding hypotension.

The kidneys are susceptible to low blood pressure, and even brief episodes of hypotension can cause AKI. We must act quickly to stabilize blood pressure and address hemodynamic instability.

Detecting and treating urine retention early.

Routinely palpate the lower abdomen for bladder distension, especially in elderly males with dementia or encephalopathy. If a Foley catheter is in place, confirm it is patent and draining properly.

Limiting the use of nephrotoxins

• Several medications may cause nephrotoxicity! NSAIDs, IV vancomycin, aminoglycosides, amphotericin B, acyclovir, methotrexate, Cyclosporins, tacrolimus, and IVIG are just some of the medications.
• Among NSAIDs, Ketorolac is the most nephrotoxic and should not be used for more than 5 days.
• IV Vancomycin and aminoglycoside levels should be closely monitored, I typically have our pharmacy handle that. We must switch to less nephrotoxic antibiotics as soon as we can.
• IV Acyclovir can cause crystal-induced nephropathy, particularly at higher doses. Ensure patients are well-hydrated before starting therapy and continue IV fluids during treatment unless contraindicated.

• Always opt for a less nephrotoxic alternative when an equally effective medication is available.
• Kidney function and urine output should be closely monitored whenever nephrotoxic medications are administered.

In patients with CKD, it’s important to avoid nephrotoxins whenever possible. NSAIDs should be avoided entirely, and contrast agents should only be used if necessary. Additionally, ensure all medications are dosed appropriately for renal impairment.

Diagnosis of AKI

AKI is an abrupt decline in kidney function, reflected by a decline in theGFR. Since direct GFR measurement isn’t practical, AKI is diagnosed based on creatinine accumulation or decreased urine output, using the following criteria:

• Increase in serum creatinine by ≥0.3 mg/dL within 48 hours.
• Increase in serum creatinine to ≥1.5 times baseline within 7 days.
• Urine output ≤0.5 mL/kg/hr for 6 hours.

I have three comments on this definition:

1. Trend Over Time Matters – AKI is diagnosed based on serial changes, not a single isolated value. Always compare current kidney function to previous results. If prior values are unavailable and the patient presents with abnormal kidney function, assume AKI until proven otherwise.
2. BUN is Not Included – Serum creatinine is the preferred marker as it more accurately reflects GFR. BUN levels can be influenced by protein intake, catabolism, GI bleeding, or liver dysfunction, making them less specific for AKI.
3. No Creatinine Cutoff – A normal BUN/Cr ratio does not necessarily mean normal kidney function, while an abnormal ratio may indicate chronic kidney disease (CKD) rather than AKI.

The underlying cause

• History and physical exams remain the single most important element in finding out the underlying cause of AKI.
  • Patients who are volume-depleted such as those with vomiting, diarrhea, decreased oral intake, and bleeding are likely to have AKI due to renal hypoperfusion or what we call prerenal AKI.
  • Patients with signs of volume overload such as peripheral edema and ascites are likely to have a prerenal AKI due to decreased effective circulatory volume. When this happens in patients with congestive heart failure with decreased cardiac output we call it cardiorenal syndrome.
  • The development of AKI in patients with decompensated liver cirrhosis suggests possible hepatorenal syndrome.
  • AKI with urine retention suggests obstructive uropathy or what we call post-renal, this is mainly seen in elderly male patients and those with urinary catheters.
  • AKI after hypotension suggests ATN! Remember that even transient episodes of hypotension can cause AKI.
  • Medications can cause AKI via different mechanisms:
    • ATN such as with vancomycin and aminoglycosides.
    • Crystal-induced nephropathy such as methotrexate, acyclovir, amoxicillin, and sulphamethoxazole.
    • AIN (Acute interstitial nephritis) such as with beta-lactam antibiotics, NSAIDs, and PPI.

• The development of AKI in the setting of rhabdomyolysis especially when CK level > 5000 suggests possible pigment-induced nephropathy. Think of rhabdomyolysis in patients with prolonged immobilized state, heat exertion, trauma, and some drugs. Remember that rhabdomyolysis may cause elevated AST/ALT as well.
• AKI that develops within 48 to 72 hours after contrast exposure suggests contrast-induced nephropathy.

W/U

Even when the cause of AKI seems clear based on the history and physical exam, I always perform a urinalysis and renal ultrasound to look for any evidence of obstruction. I reserve additional urine tests—such as FENa, FEUrea, urine creatinine, cast analysis, and sometimes renal biopsy for cases where the etiology of AKI remains unclear after my initial assessment.

Management of AKI

• When my patient develops AKI, I reflexively do these five things:
  • Discontinue any potential nephrotoxin and offending agents.
  • Correct and avoid hypotension.
  • Ask the pharmacy to renally adjust all medication.
  • Switch to a renally safe alternative if possible, for example, switch to LMWH to UFH for DVT prophylaxis or anticoagulation.
  • Palpate the patient’s lower abdomen to check for any bladder distension and place a Foley catheter if detected. This is particularly important in elderly gentlemen.

Obstructive uropathy

• The treatment of obstructive uropathy involves relieving the obstruction and managing volume and electrolytes.
• Urinary catheterization relieves the obstruction in most cases. I always consult urology with these patients.
• If the obstruction is due to BPH, alpha-blockers such as tamsulosin must be initiated.
• Volume management is crucial in these patients given potential post-obstructive diuresis.
  • There is no set rule for a fluid replacement here! Ensuring the patient remains hemodynamic stability is the main goal.
  • Some may opt to track UO and replace it with fluids, a 50–75% strategy can be used which means replacing 50-75% of the previous hour’s urine output with IV fluid.
• Post-decompression hematuria may develop with rapid bladder decompression.

Prerenal AKI

• The management of prerenal AKI depends on the cause of decreased renal perfusion.
• Volume depletion:
  • Aggressive IV fluid resuscitation with isotonic crystalloid solutions, don’t shy away from using LR or plasmalyte because of the concern of hyperkalemia!
  • Bicarb drip should be used instead if metabolic acidosis is present, I use bicarb drip when HCO3 < 22.
• Volume overload:
  • IV loop diuretics. Patients with AKI require higher doses of loop diuretics, the starting dose of furosemide is 80 mg once or twice daily, and 2 mg once or twice daily for bumetanide.

• Patients with congestive heart failure and low CO syndrome may require inotropes as well. Please consult cardiology in addition to nephrology if you decide to use inotropes.
• Albumin along with terlipressin or norepinephrine is the treatment of choice for hepato-renal syndrome.

Acute interstitial nephritis

• Discontinue any potential offending agents as this can lead to partial or complete recovery of renal function.
• If no improvement in kidney function within 5-7 days after stopping the offending drug, corticosteroids are recommended. Prednisone is commonly used, starting at 1 mg/kg/day for 1-2 weeks, followed by a taper over 4-6 weeks. Early initiation of steroids is associated with better outcomes and reduced risk of chronic kidney disease.

Acute tubular necrosis (ATN)

• Acute tubular necrosis (ATN) is probably the most common form of AKI in critically ill patients.
• It frequently results in oliguria, anuria, and the need for renal replacement therapy (RRT).

• Anuric or oligouric AKI always makes me nervous, I consult nephrology right away in these patients as life-threatening hyperkalemia and acidosis can develop quickly requiring RRT.
• Don’t be deceived by the initial normal K! As long as they are oliguric or anuric, potassium likely will rise despite hyperkalemia management, the same applies to metabolic acidosis.

Crystal-induced and pigment-induced nephropathy

The treatment of crystal-induced and pigment-induced nephropathy is similar and involves discontinuing the offending agent and providing supportive care with IV fluid resuscitation. In some cases, urine alkalinization may be necessary. Nephrology consultation is essential to optimize management and minimize the need for renal replacement therapy (RRT).

Initiating Renal replacement therapy (RRT)

• The Nephrology team typically decides when to initiate RRT, whether early or late, and whether to use CRRT or intermittent HD.
• CRRT is typically chosen in patients with hemodynamic instability who can’t handle the fluid shift used in regular HD.
• Critical hyperkalemia and severe metabolic acidosis are the two main reasons for emergent RRT in critically ill patients.

• Volume overload is another indication of RRT in ATN patients! Before starting RRT, if the patient is stable, a high-dose loop diuretic challenge can help assess responsiveness. Typically, we give IV furosemide at 1 mg/kg (or equivalent). If urine output remains ≤600 mL after 6 hours, it suggests poor response and a likely need for dialysis.
• RRT is also indicated for uremic complications such as encephalopathy, pericarditis, and bleeding. RRT is also used for some toxins removal.
• I understand that some of you may consult nephrology for every case of AKI, but that’s not always necessary. Many cases, such as AKI due to volume depletion, are straightforward and typically resolve with IV fluid resuscitation. Let’s reserve nephrology consults for more complex or severe cases, allowing them to focus on the situations that truly require their expertise!

Monitoring

• Patients with AKI should have their Urine output (UO), electrolytes, and kidney function closely monitored.
• While urine output is routinely monitored in critically ill patients, it may not be tracked as closely for those on the regular hospital floor. We must relay the importance of tracking urine output to patients and nurses.

• AKI is a dynamic process with a continuously changing GFR and creatinine clearance and for that reason, serial labs for kidney functions and electrolytes including HCO3 – labeled as CO2 on BMP/CMP- must be obtained!
  • For critically ill patients, particularly those with oliguria or anuria, key labs such as electrolytes, creatinine, and acid-base status should be monitored every 6–8 hours (or up to 12 hours, depending on clinical context). These patients are at high risk for rapid deterioration, including life-threatening hyperkalemia and metabolic acidosis. A single normal potassium (K) level or mildly elevated creatinine on a basic metabolic panel (BMP) should not provide false reassurance, as values can shift abruptly in unstable clinical conditions.
  • For stable inpatients with adequate urine output, daily laboratory monitoring is typically sufficient. However, more frequent testing (e.g., every 12–24 hours) is warranted if significant electrolyte imbalances, worsening renal function, or other clinical concerns arise.

Prognosis

• AKI due to volume depletion and obstructive uropathy resolves quickly if prompt intervention is provided.
• AKI from ATN may take weeks to months to recover, depending on the severity of tubular injury and comorbidities (e.g., diabetes, chronic kidney disease). Some patients may develop residual CKD or progress to ESRD.
• In AIN, Kidney function typically improves within weeks if the offending drug is stopped and steroids are initiated early.
• In crystal-induced nephropathy, recovery within days with early intervention including rapid hydration, urinary alkalinization, and discontinuing the offending drugs.
• In pigment-induced AKI, aggressive IV fluids to flush out nephrotoxic pigments (myoglobin, hemoglobin) can prevent permanent damage. However, severe cases may still progress to ATN or CKD.

Ordering a CT (or CAT) scan and wondering whether contrast is needed? And if you do need contrast, should it be IV or oral? Let’s make this simple for you.

In this post, we’ll break down when to order non-contrast CT, contrast CT, and the different types of contrast to consider (oral, IV, or both). You’ll have a clear framework to guide your decisions by the end.

Types of Contrast

Contrast can be administered in three ways:

• Oral contrast: Helps visualize the gastrointestinal (GI) tract.
• Rectal contrast: Occasionally used for imaging the lower GI tract.
• IV contrast: Highlights blood vessels, organs, and certain tissues.

1. When to Use Oral or Rectal Contrast

The only times you’ll need oral or rectal contrast are:

• GI perforation or anastomosis leak: Use water-soluble iodinated contrast (e.g., Gastrografin) instead of barium-based contrast.
• Distal colonic or rectal perforation/leak: Consider rectal contrast.

Important Note: Oral contrast is unnecessary for diagnosing small bowel obstruction (SBO). Use IV contrast with CT abdomen/pelvis for SBO.

2. When to Use IV Contrast

Use IV contrast for:

• Cancer: Evaluating suspicious lesions or staging.
  • Exceptions: Low-dose lung cancer screening, colon cancer screening (CT colonography), pulmonary nodule follow-up, and lymphoma assessment.
• Infections: Abscesses, empyema, osteomyelitis, septic arthritis, or infected hardware.
• Trauma with penetrating or vascular injuries. if there are no penetrating or vascular injuries then there is no need to give IV contrast
• Inflammatory conditions: Such as IBD, pancreatitis, diverticulitis, and appendicitis.
  • Exception: Interstitial lung disease (ILD) assessment with high-resolution CT (HRCT)—no IV contrast needed.
• Infarction/Ischemia: This includes kidney infarcts and ischemic bowel.
  • Exception: For brain or lung infarctions, non-contrast CT is preferred.
• Vascular conditions: Thrombosis, dissection, aneurysms, or pseudoaneurysms. Use CT angiography (requires IV contrast).

3. When to Order Non-Contrast CT

Non-contrast CT is sufficient for:

• Initial stroke evaluation.
• Hematomas: Retroperitoneal hematomas (although IV contrast can also be used).
• Kidney stones.
• Musculoskeletal issues: Fractures and spinal diseases (if infection isn’t suspected).
• Non-penetrating trauma.
• Interstitial lung disease (HRCT).
• Screenings:
  • Low-dose lung cancer screening (LDCT).
  • Coronary calcium scoring.
  • CT colonography.

4. Real-Life Clinical Scenarios

Here are practical examples to solidify your understanding:

Scenario 1: Pulmonary Embolism (PE)

A 40-year-old woman on birth control pills presents with sudden shortness of breath. PE is suspected. PE is a vascular condition.

Order: CT chest angiography with IV contrast.

Scenario 2: Diverticulitis

A 65-year-old patient with LLQ abdominal pain. Acute diverticulitis is suspected.
Acute diverticulitis is an inflammatory process.

Order: CT abdomen/pelvis with IV contrast.

Scenario 3: Trauma and Anticoagulation

An 80-year-old man on warfarin falls and sustains a head laceration. CT of head, neck, chest, abdomen, and pelvis ordered. On exam, he only had some head lacerations and no signs of other injuries.

The patient had a trauma without penetrating or vascular injuries, hematoma also needs to be ruled out as he was on anticoagulation.

Order: Non-contrast CT.

Scenario 4: Kidney Stones

A 30-year-old woman with recurrent flank pain and a history of kidney stones, and renal colic was suspected to be the culprit.

Order: Non-contrast CT abdomen/pelvis.

Scenario 5: Severe Abdominal Pain

A 45-year-old patient with severe abdominal pain and vomiting, on physical exam, his abdomen remained soft but with diffuse tenderness, The ED physician ordered CT abd/pelvis.

Order: CT abdomen/pelvis with IV contrast (oral contrast is unnecessary, particularly with vomiting).

Scenario 6: Suspected Stroke

80-year-old man with sudden aphasia. Stroke suspected.
Order: Non-contrast CT head.

Scenario 7: Infection with Hardware

58-year-old woman s/p back surgery involving hardware placement presented with back pain and surgical wound discharge. MRI is unavailable.
Order: CT lumbar spine with IV contrast (infection suspected).

Final Tips

• Always assess for contrast allergies and ensure normal kidney function before ordering contrast studies.
• When in doubt, consider the clinical scenario—contrast should add diagnostic value and improve outcomes.

The coadministration of anticoagulation and thrombolytics

Anticoagulation should be started immediately when administering thrombolytic therapy to a patient with a STEMI, we give both together. The same applies to PE with hemodynamic instability.

This is different from using thrombolytics in ischemic stroke! In ischemic stroke, the American Heart Association/American Stroke Association (AHA/ASA) guidelines recommend delaying the initiation of anticoagulation for 24 hours after thrombolytic therapy with alteplase to minimize the risk of hemorrhagic transformation.

Holding anticoagulation before procedures

Right-sided thoracentesis, paracentesis, central line placement including picc lines, diagnostic endoscopy with or without biopsy, dental procedures, minor dermatological procedures, ophthalmological procedures, and pacemaker and ICD placement are considered minor procedures and considered low risk for bleeding.

The American College of Chest Physicians guidelines support the continuation of anticoagulants for minor procedures due to their low bleeding risk. The same applies to antiplatelets.

In real-world settings, unless the procedure is emergent, I highly recommend checking with the performing physician to see if we should hold oral anticoagulants to avoid unnecessary delays! Unfortunately, not everyone goes with these guidelines for different reasons!

Suppose the performing provider wants to hold oral anticoagulants. In that case, we hold DOAC for 48 and hold warfarin until the INR falls to a level that is deemed safe by the performing physician which is typically ≤ 1.5.

Anticoagulation bridging

Bridging with UFH or LMWH is warranted in patients who are taking warfarin and have a high risk for thromboembolic disease such as mechanical heart valves, AF patients with recent stroke or TIA, recent DVT or PE, and patients with known hypercoagulable status.

Bridging is initiated when the INR falls below the therapeutic range typically less than 2.

LMWH is preferred over UFH in bridging given its more predictable anticoagulation effect and should be stopped 24 hours before the procedure, If UFH is used instead, it should be stopped 4-6 hours before the procedure.

Resuming oral anticoagulants

Oral anticoagulants should be resumed after the procedure and I always ask the performing physicians if it is safe to resume. DOAC can be simply resumed, and the same applies to warfarin if bridging isn’t indicated. If bridging was indicated, it should continue until the INR is therapeutic. Here’s the transitioning strategy we follow:

• From UFH: Start the DOAC at the time of heparin drip discontinuation.
• From LMWH: Start the DOAC when the next LMWH dose is due.
• No loading dose is needed when resuming a DOAC—simply restart the home dose.

Heparin-induced thrombocytopenia

HIT is a serious condition with significant morbidity and mortality if untreated and one should not wait for thrоmbоsis to develop before suspecting НΙТ because thrοmbοϲуtοpeոiа often precedes that.

Calculating the 4T score is the first step when suspecting HIT. this score is a clinical tool used to estimate the probability of heparin-induced thrombocytopenia (HIT). It evaluates four parameters related to HIT and stratifies patients into low, intermediate, or high probability categories. This scoring system helps guide further diagnostic testing and management. You don’t need to memorize it, just use one of the free online calculators.

If the 4 Ts score is a low probability, we generally do not pursue HΙΤ antibody testing or presumptive treatment for НІΤ, we do not discontinue hepariո or start a non-heparin anticoagulant

If the 4 Ts score is an intermediate or high probability, we make a presumptive diagnosis of ΗІТ pending results of НΙT antibody testing.

Нерariո cessation alone is not sufficient since patients with НΙТ remain at risk for subsequent thrоmbοsis. So If you decide to test for HIT, you must act pending test results.

Testing for HIT starts with screening antigen assay tests like ELISA, which detect antibodies against platelet factor 4 (PF4)/heparin complexes. These assays are fast and highly sensitive but have moderate specificity, leading to potential overdiagnosis.

A negative result will rule out HIT, but if positive we send a confirmatory functional assay unless the clinical suspicion is high then there is no need.

Non-heparin anticoagulants include argatroban, bivalirudin, fondaparinux, or a direct oral anticoagulant (DOAC). Remember the use of Fodaparinux and DOAC in HIT is considered off-label.

Argartroban and bivalirudin have short durations of action and are good choices for critically ill patients. Argatroban is safe in renal insufficiency, while bivalirudin is good in liver dysfunction.

Fondaparinux is a good and easier-to-use option but is contraindicated in patients weighing less than 50 kg and those with a creatinine clearance below 30 ml/min. It’s also best avoided when the platelet count is below 50,000/µL.

DOAC agents are best used in stable patients, they are equally effective. Apixaban is the DOAC of choice in renal insufficiency and dialysis patients. A loading dose of DOAC is required similar to treating venous thromboembolic disease.

In cases HIT is confirmed, the duration of anticoagulation therapy should be at least 4 weeks for isolated HIT and 3 months for HIT with thrombosis.

In the case of using Argatroban and Bivalirudin, have your pharmacist help with their protocol and monitoring and transition to oral anticoagulants once the patient is stable preferably DOAC, if you decide to transition into warfarin we must overlap until the INR is therapeutic for at least 24 hours.

Anticoagulation reversal

For warfarin-associated life-threatening bleeding, 4-factor Prothrombin Complex Concentrate (4-factor PCC) which contains factors II, VII, IX, and X is the first-line reversal solution, if not available, we can use the combination of 3-factor PCC and factor 7 as factor-3 PCC lacks factor 7. FFP is used when PCC solutions are not available.

In most cases, the goal is to bring INR to ≤ 1.5. Check the INR level 15-30 minutes after completion of the infusion and repeat the infusion until INR is ≤ 1.5, repeat the infusion if INR is still elevated.

In general, it is reasonable to consider restarting anticoagulation therapy 7 to 14 days after an episode of major bleeding.

Final approval should always be secured from the subspecialists overseeing the bleeding management.

For DOAC reversal, we follow the following strategy:

• Dabigatran: Idarucizumab is the first line, or PCC/aPCC, if Idarucizumab is unavailable. If PCC is not available then HD may be considered to remove the drug as the next step.

• Factor Xa inhibitors (rivaroxaban, apixaban, edoxaban): Andexanet alfa (preferred), or PCC/aPCC if andexanet alfa is unavailable.

Protamine sulfate is the primary agent to reverse the anticoagulation effect of UFH and LMWH in life-threatening bleeding.

Anticoagulation and bleeding

In cases of significant bleeding, the immediate priority is to discontinue all anticoagulation. The next step is to reverse the coagulopathy when clinically appropriate.

In cases of minor bleeding, such as gum bleeding, epistaxis, bloody stools from inflammatory bowel disease (IBD), microscopic hematuria, or hemoptysis caused by a lung abscess, anticoagulation can often be continued with caution. However, addressing the underlying cause of the bleeding is essential. Importantly, if hemoptysis is due to pulmonary embolism (PE), anticoagulation should not be withheld, as treating the PE is the priority.

n thrombocytopenia is drug-induced, plt transfusion is indicated in active bleeding to keep the plt count above 50k.

Anticoagulation can be resumed 7-14 days after a major bleeding episode.

For anticoagulation in critically ill patients and those at high rebleeding risk, UFH infusion is preferred given its short duration of action. LMWH or DOAC can be considered when the patient becomes more stable and low bleeding risk.

A platelet count of ≥ 50k is considered safe to start anticoagulation, a lower threshold of ≥ 30k can be considered if the benefit outweighs the risk of starting anticoagulation.

The IVC filter debate

The use of inferior vena cava (IVC) filters is a topic of considerable debate in the medical community. IVC filters are indicated primarily for patients with venous thromboembolism (VTE) who have an absolute contraindication to anticoagulation or in those who have recurrent VTE despite adequate anticoagulation. This recommendation is supported by the American Society of Hematology (ASH) and the Society of Interventional Radiology, among others.

However, there are significant concerns regarding the routine use of IVC filters due to the associated risks and limited evidence of long-term benefits. Studies have shown that while IVC filters can reduce the incidence of pulmonary embolism (PE) in the short term, they are associated with an increased risk of deep vein thrombosis (DVT) and other complications such as filter migration, perforation, and thrombosis.

The American Society of Hematology guidelines conditionally recommend against the use of IVC filters in patients who can be safely treated with anticoagulant therapy, citing low certainty in the evidence of their effects. Similarly, the Society of Interventional Radiology advises that IVC filters should be used selectively and recommends the use of retrievable filters, with removal once the patient can be safely anticoagulated.

In summary, while IVC filters have a role in specific clinical scenarios, their use should be carefully considered, weighing the potential benefits against the risks. The current consensus advises against their routine use in favor of anticoagulation whenever possible.

Recognizing hypoxic patients

Most critically hypoxic patients exhibit early warning signs of mild hypoxia before deteriorating. Recognizing and addressing these early signs can save lives and prevent the severe complications associated with untreated hypoxia.

“O2 sat reading is an essential part of vital signs and must always be mentioned along with whether on RA or O2 supplement and how much supplement the patient is on”

Take a look at patients A and B, can you tell who is more hypoxic?

You can see that patient A is worse than B despite the O2 sat of patient A being better than B because patient A requires 10 L compared to none in patient B.

The moment I observe any of the following conditions, I need to determine the cause and address the underlying issue promptly:

• RA O2 sat < 95%.
• A patient who does not normally use home oxygen but now requires supplemental oxygen to maintain an O2 saturation of 95% or higher.
• A patient who normally uses home oxygen but now requires a higher oxygen flow than their usual baseline.

By doing this, you can prevent most patients from deteriorating due to untreated progressive hypoxia, effectively saving their lives!

We also need to pay close attention when nurses call about an oxygen-related issue. They may not explicitly mention a problem with oxygenation because, like physicians, nurses may vary in experience and may not always convey a sense of urgency. Let me provide some examples of what they might say during such calls:

• Hey doc, I am having a hard time keeping the patient’s O2 saturation up, I have to increase his O2 to 8 L/m but he’s doing better now.
• Hey doc, nothing urgent! I forgot to tell you that I have to crank the patient’s O2 a bit up but he’s doing okay now and his O2 sat is in the 90s
• Hey doc, my patient’s O2 sat dropped to low 80% a while ago, I put him on 2 L/min and it quickly improved to 92%, just wanted to let you know
• And of course, they may tell you straight to come and see the patient immediately because of very low O2 saturation

In all these scenarios, I always ask the nurse for the exact current pulse oximetry reading, the amount of oxygen the patient is receiving, a full set of vital signs, and how the patient is feeling. Then, I immediately go to evaluate the patient in person.

Stabilizing hypoxic patients

The moment I suspect, smell, or know my patient is hypoxic, I have to correct this hypoxia ASAP!

We categorize patients into:

• Stable patients: These are the patients whose nurses have already increased their oxygen supplementation and now have an O2 saturation above 92%, are asymptomatic, and have stable vital signs. They still need to be evaluated promptly to determine the cause of their increased oxygen requirement and to address it appropriately, preventing future deterioration.
• Unstable patients: O2 sat is low, they are symptomatic, and the rest of the vital signs are unstable, this is a medical emergency, leave everything and go see your patient, Over the phone, I instruct the nurse to increase the patient’s oxygen supplementation to the maximum capacity of the available oxygen delivery device. At a minimum, the patient should be placed on a 100% non-rebreather mask. If the patient is already on BiPAP, CPAP, or HFNC, I direct them to increase the FiO2 to 100%.

 

“Remember to activate the RRT if you have it at your hospital to speed up the response to your patient”

Upon entering the room, I ensure the patient is receiving the maximum oxygen supplementation available at the bedside, is connected to a monitor, the crash cart is nearby, and defibrillator pads are applied. If the Rapid Response Team (RRT) is activated, these steps should already be in place.

Proceed with endotracheal intubation immediately if hypoxic respiratory failure is associated with:

• Encephalopathy, whether the patient is agitated, lethargic, or obtunded. Begin bag-valve-mask ventilation immediately if the patient is extremely lethargic or obtunded.
• Recurrent aspiration due to persistent vomiting.

In these situations, don’t hesitate—proceed with intubation immediately.

If the patient is not encephalopathic, rapid action is still crucial to prevent further deterioration and, if possible, avoid the need for mechanical ventilation.

Quickly assess the patient by listening to their lungs (if possible), checking for any fluids or blood products being administered, and gathering a brief history from the nurse. Then, position yourself at the foot of the bed to take control of the situation. All of this should be accomplished within 30 seconds.

If the patient’s O2 saturation remains below 90-92%, escalate to the highest level of oxygen delivery available. Here’s what I mean:

At my facility, we have a high-flow nasal cannula (HFNC), CPAP, and BiPAP, all capable of delivering 100% FiO2. The choice between them depends on the underlying condition:

• Choose BiPAP over CPAP or HFNC if there is confirmed or suspected hypercapnia (e.g., COPD or obesity hypoventilation syndrome) based on ABG results or clinical suspicion. Use BiPAP until ABG results are available.
• Choose CPAP or HFNC for pure hypoxia without hypercapnia:
  • CPAP is preferred if the patient has significant respiratory distress or increased work of breathing.
  • HFNC is ideal if the patient cannot tolerate a mask, has facial injuries, or is at high risk of aspiration.

In the heat of the moment, choosing any of these devices is acceptable. If you’re feeling stressed or overwhelmed and can’t decide, default to any device—it will suffice until the patient stabilizes.

Remember, during this acute phase, I’m less concerned about inappropriately reducing CO2 (hypocapnia) because it isn’t immediately life-threatening. Hypoxia, however, can be fatal

What settings should we use?

Regardless of the device chosen, all patients should initially be placed on 100% FiO2. Here’s how to set up each device:

• HFNC (High-Flow Nasal Cannula):
  Specify the flow rate in addition to FiO2. The maximum flow rate depends on the machine’s brand. For example, at our hospital, we use Vapotherm, which allows a maximum flow rate of 40 L/min. Start with the maximum flow rate.
• CPAP (Continuous Positive Airway Pressure):
  Set the CPAP value. A good starting point is 10 cmH2O.
• BiPAP (Bilevel Positive Airway Pressure):
  Set both the EPAP (equivalent to CPAP) and IPAP values:
  • Start with an EPAP of 10 cmH2O.
  • For the IPAP, add 5 cmH2O to the EPAP to achieve a PIP (peak inspiratory pressure) that is 5 cmH2O higher than the EPAP. For instance, begin with 10/15 (EPAP of 10 cmH2O and IPAP of 15 cmH2O).

These initial settings provide effective oxygenation and ventilation while allowing for quick adjustments based on the patient’s response.

There are two ways to improve oxygenation:

1. The quick way: Increase the FiO2.
2. The gradual way: Increase the flow rate on HFNC, the CPAP value on the CPAP machine, or the EPAP on the BiPAP machine.

It’s important to note that only BiPAP can assist with ventilation due to the pressure difference between IPAP and EPAP.

Remember, oxygen saturation may not improve immediately. Stay calm—it can take several minutes for O2 saturation or pO2 levels to increase. As long as there is steady improvement, you can be reassured.

If the O2 saturation isn’t improving or is declining despite being on maximum HFNC, switch to CPAP or BiPAP using the previously recommended settings. If the patient is already on CPAP or BiPAP, consider increasing the CPAP or EPAP value in increments of 2-3 cmH2O. For BiPAP, ensure that the IPAP is adjusted to maintain a PIP at least 5 cmH2O above the EPAP.

When to consider intubation and mechanical ventilation in patients who are not encephalopathic?

The decision to proceed with mechanical ventilation isn’t always clear-cut, multiple factors need to be considered including code status, mental status, and hemodynamic stability.

In general, mechanical ventilation should be strongly considered if a patient’s oxygen saturation remains below 80% despite maximum oxygen support and there are no signs of clinical improvement. However, during the COVID era, we encountered patients with oxygen saturations in the 70s who were managed without intubation. Always use your clinical judgment to guide the decision.

Let’s compare two examples:

• Patient A initially had an oxygen saturation in the 40s. After being placed on CPAP at 10 cmH2O with 100% FiO2, their O2 saturation began to progressively improve, reaching the high 60s and continuing to rise. For this patient, I would give more time, as their oxygen levels are steadily improving with oxygen therapy and treatment of the underlying cause.
• Patient B started with oxygen saturation in the low 80s, but despite CPAP at 10 cmH2O with 100% FiO2, their O2 levels continued to decline, dropping to the 60s and then the 50s. This patient will require intubation and mechanical ventilation to stabilize their condition.

Don’t hesitate to ask the people around you if we should proceed with intubation including your colleagues or nurses.

Workup and Management of the underlying cause

When stabilizing a patient’s oxygenation, it’s equally important to investigate the underlying cause. Here’s a step-by-step framework:

Initial Steps to Stabilize and Investigate

1. Gather a brief history from the patient’s nurse.
2. Listen to the patient’s lungs for clues.
3. Inspect the room for IV fluids or blood products being administered.
4. Order essential diagnostics:
   • Stat chest X-ray (CXR)
   • Electrocardiogram (EKG)
   • Arterial blood gas (ABG)

Understanding the Causes of Acute Hypoxemia

While hypoxemia can result from five mechanisms—hypoventilation, V/Q mismatch, right-to-left shunt, diffusion limitations, and low-inspired FiO2—clinical practice often reveals a more focused list of causes.

Suspect one of the following Conditions in patients who develop sudden shortness of breath and severe acute hypoxic RF:

• Pulmonary edema (cardiogenic or non-cardiogenic)
• Pulmonary embolism (PE)
• Aspiration pneumonia
• Pneumothorax (PTX)
• Lung collapse or atelectasis
• Large pleural fluid collection (e.g., pleural effusion, empyema, or hemothorax)

Breaking Down the Conditions

1. Pulmonary Edema

• Clues to Diagnosis:
  • Orthopnea, crackles on lung exam, jugular venous distension (JVD), peripheral edema.
  • Presence of IV fluid or blood product infusions.
• Management:
  • Stop IV fluid or blood product infusions immediately.
  • Administer 80 mg IV furosemide.
  • Use CPAP if no CO2 retention is suspected.
  • Start a nitroglycerin drip if blood pressure is elevated.
  • Perform diagnostics: EKG, chest X-ray, cardiac enzymes, and echocardiogram.

2. Aspiration Pneumonia

• Clues to Diagnosis:
  • Reports of choking or visible vomiting around the mouth or bed.
• Management:
  • Proceed with intubation if the patient is actively vomiting or aspirating.
  • If intubation isn’t required immediately, initiate HFNC at maximum settings.
  • Avoid CPAP/BiPAP if the patient cannot clear secretions unless a nasogastric tube (NGT) is placed for suction.
  • Start antibiotics to address potential infection.

3. Pneumothorax, Atelectasis, or Large Pleural Fluid Collection

• Pneumothorax (PTX):
  • Clues: Absent breath sounds on one side.
  • Management:
    • Confirm diagnosis with CXR and place a chest tube immediately.
    • For tension PTX, perform needle decompression if chest tube placement is delayed.
    • Use maximum HFNC to manage hypoxia until a chest tube is in place.
• Atelectasis:
  • Clues: Weak cough, difficulty clearing secretions, tracheal shift toward the affected side.
  • Management:
    • Initiate chest physiotherapy (CPT), suctioning, mucolytics, and breathing treatments.
    • If no improvement, consult pulmonary for bronchoscopy.
• Large Pleural Space Collection:
  • Clues: Tracheal shift toward the unaffected side.
  • Management:
    • Perform therapeutic thoracentesis, ideally with chest tube placement.
  • Key Considerations:
    • Pleural effusion: Common with malignancy, cirrhosis, or heart failure.
    • Empyema: Severe leukocytosis, pleuritic chest pain, systemic illness.
    • Hemothorax: Often linked to trauma or thoracic procedures.

4. Pulmonary Embolism (PE)

• When to Suspect:
  • Hypoxia unexplained by lung exam or CXR findings.
• Management:
  • If suspicion is high and there are no contraindications, start full anticoagulation immediately.
  • Obtain a chest CTA, but ensure the patient is stable enough for the scan.
  • Use bedside POCUS to assist in diagnosis if trained.

For all these patients, keep them NPO (nothing by mouth) until they are more stable. If aspiration was the underlying issue, request a speech therapy evaluation. Transfer the patient to a higher level of care, typically the ICU; however, an IMC (Intermediate Care Unit) or step-down unit may be appropriate for select patients. A comprehensive panel of blood tests is usually ordered, including:

• CBC (Complete Blood Count)
• CMP (Comprehensive Metabolic Panel)
• Cardiac enzymes
• Lactic acid

This ensures thorough assessment and monitoring of their clinical status.

Ensure continued treatment and monitoring as needed based on the patient’s condition. For example:

• Administer additional diuretics for persistent pulmonary edema.
• Perform more frequent chest physiotherapy (CPT) or consider bronchoscopy if indicated.
• Confirm that a chest CTA is completed and promptly follow up on the results if PE is suspected.

Adjust care dynamically to address the evolving clinical situation.

Further workup and treatment may be necessary based on the findings. For instance, if the EKG indicates evidence of an acute MI, follow the appropriate treatment guidelines.

Ensure to order a follow-up ABG and adjust treatment as needed. As the patient stabilizes:

• Gradually wean FiO2 down as tolerated.
• Avoid reducing the flow rate on HFNC or the CPAP/EPAP values until FiO2 is decreased to 60%. Once FiO2 is at this level, begin weaning both the FiO2 and flow/pressure settings together.

This approach helps optimize oxygen delivery while ensuring patient safety during recovery.

The end

Deep vein thrombosis (DVT) prophylaxis is crucial in hospitalized patients. Still, the choice of therapy depends heavily on individual patient factors such as renal function, bleeding risk, mobility, and underlying conditions. In this post, we’ll explore real-world scenarios highlighting the common pitfalls of DVT prophylaxis. For the record, we are specifically talking about adult medical patients. Orthopedic and non-orthopedic surgical patients have a bit different guidelines.

1st scenario:

A 60-year-old gentleman with a PMH of hypertension and type 2 diabetes was admitted with community-acquired pneumonia and acute hypoxic respiratory failure, lab data showed normal kidney function and normal platelet count, and the patient was started on Heparin 5000 units SQ TID.

Comments: Low-molecular-weight heparins (LMWH), such as enoxaparin or dalteparin, are the preferred anticoagulants for preventing deep vein thrombosis (DVT) based on evidence from randomized trials showing their superiority. UFH is reserved for situations where LMWH is unsuitable, such as in dialysis-dependent patients, those with acute kidney injury (AKI), or when LMWH is unavailable. I included AKI here because of its dynamic nature, where rapidly changing kidney function leads to fluctuating creatinine clearance. Once kidney function stabilizes, switching back to LMWH is appropriate! So this patient should’ve been started on a LMW heparin. If the patient is allergic to heparin and heparin derivatives Fondaparinux or DOAC can be alternatively used, more on that soon!

Scenario 2:

A 21-year-old healthy gentleman presented with intractable nausea and vomiting, UDS was positive for cannabis, he was admitted for symptom control, labs were unremarkable, and Enoxaparin 40 mg daily was ordered.

Comment: Patients who are fully ambulatory and expected to have a short hospital stay are considered low-risk and typically do not require DVT prophylaxis. This patient met these criteria and was therefore deemed low risk for developing thromboembolic disease, so DVT prophylaxis was not needed in this case.

DVT prophylaxis is recommended for patients at moderate or high risk. While several scoring systems can help assess risk, my approach is straightforward: if a patient is not fully ambulatory and their hospital stay is expected to be longer than 24 hours, I provide DVT prophylaxis.

Scenario 3:

A 72-year-old lady, who’s on HD three times a week, was admitted with intractable nausea and vomiting, her labs showed Hemoglobin of 7.3 and plt count of 250k, the patient was started on IV fluid and placed on intermittent pneumatic compression for DVT prophylaxis.

Comment: When DVT prophylaxis is indicated, the sole use of mechanical DVT prophylaxis in the absence of contraindications to chemical methods is inappropriate. Mechanical methods—such as intermittent pneumatic compression (IPC), graduated compression stockings (GCS), and venous foot pumps—are primarily indicated for patients who have a high risk of bleeding or in whom anticoagulation is contraindicated. This patient should have been started on chemical DVT prophylaxis, specifically unfractionated heparin, as low molecular weight heparins are typically avoided in dialysis patients.

Adding a mechanical method to chemical DVT prophylaxis is acceptable, especially in patients at high risk for DVT. High-risk patients include those with a history of previous thromboembolic disease, cancer, and stroke.

Scenario 4:

A 55-year-old gentleman with a history of pancreatic cancer presented with intractable vomiting and diarrhea, his labs showed evidence of AKI with a calculated creatinine clearance of 29 ml/min, CBC showed plt count of 32k, and the patient was placed on intermittent pneumatic compression.

Comment: The patient is at high risk for thromboembolic disease due to his underlying pancreatic cancer, a chemical DVT prophylaxis is the most appropriate but he has a critical thrombocytopenia, and that’s why he was probably placed on a mechanical method instead of chemical prophylaxis! Generally, a platelet count of ≥50,000/μL is considered safe for anticoagulation. However, because of the patient’s high risk for DVT from his underlying cancer, the potential benefit of DVT prevention may outweigh the bleeding risk. In such high-risk cases, a lower platelet threshold can sometimes be acceptable; anticoagulation may be considered with a platelet count >30,000/μL, and in select cases, even >20,000/μL. In this situation, it would be wise to consult the patient’s oncologist to weigh the benefits and risks of chemical prophylaxis and to determine the most appropriate anticoagulant.

The patient has acute kidney injury with a creatinine clearance of less than 30 ml/min, Technically Enoxaparin or Dateparin can be used at reduced renal doses, but as we mentioned earlier, AKI is a dynamic with continuously changing creatinine clearance due to rapidly changing kidney function. Unfractionated heparin would be the most appropriate chemical prophylaxis, we can switch back to LMW heparin once kidney function is stabilized!

Scenario 5:

A 45-year-old morbidly obese man (BMI 42) with a history of coronary artery disease (CAD) and recent percutaneous coronary intervention (PCI), currently on dual antiplatelet therapy (DAPT), was admitted with acute sigmoid diverticulitis. His labs were unremarkable, and his provider did not prescribe chemical DVT prophylaxis, assuming DAPT would suffice.

Comment: Although DAPT reduces the risk of arterial thrombosis, it does not offer adequate protection against venous thromboembolism (VTE). Therefore, chemical DVT prophylaxis is still recommended for this patient. Low molecular weight heparin (LMWH) would be a suitable choice, but special attention must be given to dosing in morbidly obese patients, as standard doses may be inadequate.

Dosing Recommendations for Patients with BMI ≥40 kg/m²:
Patients with a BMI >40 kg/m² require higher doses of DVT prophylaxis due to pharmacokinetic changes in obesity. Standard doses may lead to subtherapeutic anticoagulation levels, necessitating adjusted dosing as follows:

• Enoxaparin:
  • Standard dose: 40 mg subcutaneously (SQ) once daily.
  • If creatinine clearance (CrCl) is <30 mL/min, reduce to 30 mg SQ daily.
  • In patients with BMI ≥40, increase to 40 mg SQ twice daily or consider weight-based dosing at 0.5 mg/kg once daily.
• Dalteparin:
  • Standard dose: 5000 units SQ daily.
  • For patients with BMI ≥40, increase to 7500 units SQ daily.
  • Avoid dalteparin in patients with CrCl <30 mL/min due to accumulation risk.
• Unfractionated Heparin (UFH):
  • Standard dose: 5000 units SQ twice or three times daily (TID).
  • Evidence suggests TID dosing does not significantly improve DVT prevention over BID dosing and is associated with an increased bleeding risk.
  • For patients with BMI ≥40, increase to 5000-7500 units TID, with no renal dose adjustment required.

Scenario 6:

A 55-year-old diabetic woman was admitted for pain control due to intractable back pain from a herniated disk. Her chart lists an allergy to heparin, so you asked her about the nature of the allergy. She couldn’t recall specific details but mentioned that it might have been related to a low platelet count she had in the past. Her current lab results show a platelet count of 250,000/µL and normal kidney function.

Comment:

In cases of reported heparin allergy, it’s essential to consider the possibility of a prior episode of heparin-induced thrombocytopenia (HIT), even if the exact details are unclear. Unless HIT can be definitively ruled out, it’s best to avoid both heparin and low-molecular-weight heparin (LMWH) due to the risk of exacerbating HIT. Suitable anticoagulation options in this case include fondaparinux or a direct oral anticoagulant (DOAC).

Unlike heparin, fondaparinux is structurally distinct and doesn’t carry the same HIT risk. The prophylactic dose is 2.5 mg subcutaneously once daily, which is effective even for morbidly obese patients. However, fondaparinux is contraindicated in patients weighing less than 50 kg and those with a creatinine clearance below 30 ml/min. It’s also best avoided when the platelet count is below 50,000/µL.

Alternatively, oral rivaroxaban 10 mg once daily or apixaban 2.5 mg twice daily can be used. Apixaban is a safer option if the creatinine clearance is less than 15 ml/min and in acute kidney injury (AKI).

F/U: The next day, the patient asked you how long she would need to continue the blood thinner.

VТЕ prophylaxis should ideally continue until the patient is fully ambulatory or discharged from the hospital.

Scenario 7:

A 75-year-old diabetic and hypertensive lady presented with a left-sided weakness started 30 minutes before ED arrival, the patient was evaluated in the ED and deemed a candidate for thrombolytic therapy, brain MRI was done the next morning and showed an ischemic stroke in the right MCA territory with punctate hemorrhage in the ischemic tissue, lab data was unremarkable, the stroke coordinator asked the caring provider on day 2, why the patient isn’t started on a chemical DVT prophylaxis and he indicated it’s contraindicated because of the punctate hemorrhages.

Comment: Stroke patients are at high risk for DVT and prophylaxis must be provided, in cases where thrombolytic therapy is given chemical prophylaxis should be started 24 hours after administering the thrombolytic therapy. Punctate hemorrhages seen in ischemic strokes are not considered a hemorrhagic transformation, they occur as a result of ischemic damage to blood vessels, making them more prone to minor leakage, and they are not contraindications for anticoagulation. This patient can be safely started on a LMW heparin.

How about patients with brain tumors? Brain tumors whether primary or metastatic are not absolute contraindications for chemical DVT prophylaxis, these patients are at increased risk of thromboembolic diseases, and the decision must be individualized based on their intracranial bleeding risk and overall general bleeding risk. Consulting with the patient’s neurosurgeon or oncologist is the easiest and best way to make such a decision! The same applies to spinal tumors. If you can’t reach the patient’s oncologist/neurosurgeon, place the patient on mechanical prophylaxis until you can.

How about intracranial hemorrhage? Mechanical DVT prophylaxis must be started on admission, and we add chemical prophylaxis for most patients one to four days after ΙCΗ stability is documented and confirmed by the caring neurosurgeon! An exception would be patients evaluated for urgent surgery for whom chemical prophylaxis may be temporarily withheld. I always call neurosurgery and ask them if it is safe to start a chemical prophylaxis.

Scenario 8:

A 35-year-old male with a 5-year history of ulcerative colitis, previously managed with corticosteroids and mesalamine, presents with a 3-day history of worsening abdominal pain and frequent bloody diarrhea (10 episodes/day). CBC showed HGB of 9 gm/dl and platelet count of 200k, He was diagnosed with a UC flare and started on IV corticosteroids and IV fluids. The patient was placed on mechanical DVT prophylaxis due to his bloody diarrhea.

Comment: Bloody stool in ulcerative colitis (UC) or Crohn’s disease is not an absolute contraindication for deep vein thrombosis (DVT) prophylaxis. Inflammatory bowel disease (IBD) patients are at a significantly increased risk of venous thromboembolism (VTE), especially during flare-ups, due to both inflammation and immobilization. A chemical DVT prophylaxis unless the bleeding is overt leading to critical anemia.

Scenario 9:

A 42-year-old gentleman with a history of alcoholic liver cirrhosis presented with abdominal pain and distention, his labs showed a platelet count of 55k, HGB of 8.2, and INR of 2.4, BUN/Cr of 9/0.6, the caring provider ordered Enoxaparin 40 mg SQ daily for DVT prophylaxis, the pharmacist called back asked if we want to continue with Enoxaparin as his INR was 2.4 and platelet count of 55k.

Comment: In chronic liver disease and cirrhosis, an elevated INR does not accurately reflect the patient’s coagulation status. The liver synthesizes both procoagulant and anticoagulant factors, and liver dysfunction decreases both. As a result, an elevated INR in these patients does not necessarily indicate a true bleeding risk or coagulopathy. The platelet count is above 50k which is considered safe as we discussed earlier, therefore a chemical DVT prophylaxis is indicated, and LMW heparin should be ordered given his intact kidney function.

To wrap up:

• Fully ambulatory patients with a short anticipated hospital stay are considered low risk and generally do not require DVT prophylaxis. This group typically includes young, healthy individuals. For patients who do not meet these criteria, DVT prophylaxis is recommended, provided there are no contraindications.
• LMW heparin agents are superior to unfractionated heparin and should be used except in dialysis-dependent patients where unfractionated heparin should be used. In AKI, unfractionated heparin is preferred given the dynamic nature of AKI and the continuously changing creatinine clearance.
• For patients with a history of HIT, fondaparinux and DOAC can be used. In advanced renal impairment and dialysis patients, Apixaban can be alternatively used.
• Patients with a BMI >40 kg/m² require higher doses of DVT prophylaxis due to pharmacokinetic changes in obesity.
• Punctate hemorrhages can be seen in ischemic strokes and are not considered a hemorrhagic transformation and they are not considered a contraindication for anticoagulation.
• Brain tumors whether primary or metastatic are not absolute contraindications for chemical DVT prophylaxis, the decision must be individualized based on their intracranial bleeding risk and overall general bleeding risk. Consulting with the patient’s neurosurgeon or oncologist is the easiest and best way to make such a decision!
• For intracranial hemorrhage, chemical prophylaxis should be considered one to four days after ΙCΗ stability is documented and confirmed by the caring neurosurgeon!
• Bloody stool in ulcerative colitis (UC) or Crohn’s disease, hemoptysis due to lung abscess or PE, epistaxis, microscopic hematuria, and menstrual bleeding are not considered contraindications for anticoagulation.
• In chronic liver disease and cirrhosis, an elevated INR does not accurately reflect the patient’s coagulation status and isn’t considered a contraindication for anticoagulation.

Introduction

• Blood can be transfused either as whole blood or as individual blood components.
• Blood is made of plasma, RBCs, WBCs, and platelets.
• Plasma makes up about 55% of whole blood, it’s acellular and contains water, electrolytes, proteins (like clotting factors and albumin), hormones, waste products, and antibodies.
• RBCs comprise 40-45% of the whole blood, and WBCs and platelets comprise the rest.

Whole blood transfusion

Whole blood transfusion carries the risk of volume overload, immune reactions including GVHD, and febrile reactions! In addition, whole blood has a much shorter shelf life, and WBCs and platelets lose function over time. For these reasons, whole blood transfusion is rarely used nowadays! Instead, We transfuse the individual blood components.

Packed RBCs transfusion

• Indications for PRBC transfusion vary depending on the patient’s condition:
  • Stable, nonbleeding, and asymptomatic patients: transfusion is indicated when hemoglobin (Hgb) is below 7 g/dL, multiple clinical trials including the relatively recent MINT trial support this restrictive transfusion strategy even in acute MI.
  • Patients with active bleeding and/or hemodynamic instability: RBC transfusion should continue until bleeding is controlled and hemodynamic stability is achieved, regardless of the hemoglobin level.
• Don’t be misled by the initial hemoglobin level in patients with active bleeding. This value is often falsely elevated due to hemoconcentration and only reflects the level at the time of blood draw. The true hemoglobin is likely much lower!
• In hemodynamically unstable patients, blood can be transfused as quickly as possible, similar to an IV fluid bolus.
• Each PRBC unit is about 300 ml and can be administered over 20–30 minutes, multiple units can be administered simultaneously.
• In cases where volume overload is a concern, an IV loop diuretic may be administered during or immediately after the transfusion.
• In stable patients, the PRBC unit can be transfused over 4 hours in patients at risk of volume overload, and over 2-4 in patients without that risk.
• HD patients may receive the transfusion during HD in nonemergent situations.
• O-negative blood is the fastest option in emergencies requiring packed red blood cells (PRBCs). Immediately order O-negative blood and request a type and crossmatch for the estimated number of units needed. A type and crossmatch differs from a type and screen:
  • Type and Crossmatch: Determines the patient’s ABO and Rh blood type and tests the patient’s blood against specific donor units to ensure compatibility.
  • Type and Screen: Identifies the patient’s ABO and Rh blood type and screens the patient’s serum for any clinically significant antibodies.
  • Use a type and crossmatch when transfusion is highly likely or urgent. A type and screen is appropriate when transfusion is possible but not certain.
• Wait at least 15 minutes after the transfusion is complete before drawing blood to repeat the H/H. This applies to all kinds of transfusion.

Platelet transfusion

• Platelet transfusion is indicated in the following situations:
  • Actively Bleeding Patients if plt count < 100k in CNS bleeding and < 50k for bleeding outside the CNS.
  • Before Major Surgeries if plt count < 100k in CNS surgeries and < 50k in major surgeries outside the CNS.
  • Disseminated Intravascular Coagulation (DIC) when platelet count is less than 10,000/µL to minimize serious bleeding risk.
• Avoid platelet transfusion in conditions characterized by platelet destruction, such as Immune Thrombocytopenic Purpura (ITP), Thrombotic Thrombocytopenic Purpura (TTP), Hemolytic Uremic Syndrome (HUS), and HELLP syndrome, transfused platelets are often rapidly destroyed, providing limited benefit. However, in cases of significant or life-threatening bleeding, platelet transfusions may be considered to help control hemorrhage.
•  Platelets are either obtained from a single donor by a process known as apheresis, or from Whole blood (WBD) pooled рlatеlеts (Multiple donors).
• A single donor unit roughly equals 6 to 8 random donor platelet units and is expected to raise the platelet counts by 30000/microL.

• Unlike PRBCs, platelets ABO compatibility is preferred but not necessary, ABO incompatible platelets can be used with minimal risk. However major compatible platelet transfusions are associated with higher count increments.
• RhD-negative girls or women of childbearing age must receive prophylaxis with Rh immune globulin (RhIg) if they receive platelets obtained from RhD-positive donors.

Plasma Transfusion

• Fresh frozen plasma (FFP) is indicated in INR reversal and plasma exchange.
• INR reversal is indicated in:
  • Wаrfariո-associated life-threatening bleeding
  • Before emergent or urgent procedures.

• For warfarin-associated life-threatening bleeding:
  • 4-factor Prothrombin Complex Concentrate (4-factor PCC), which contains factors II, VII, IX, and X, is the first-line reversal solution.
  • 3-factor PCC and factor 7 combination can be used if 4-factor PCC isn’t available. 3-factor PCC lacks factor 7.
  • FFP is used when PCC solutions are not available.
• FFP has a greater impact on INR at higher INR levels; as INR approaches normal, each unit’s effect diminishes. This means it takes less FFP amount to reduce the INR from 6 to 5 than from 4 to 5.
•  Each unit of FFP is 200-300 ml. Effective hemostasis generally requires coagulation factors at 25–30% of normal levels and fibrinogen levels of at least 75–100 mg/dL. To achieve this, about one-quarter to one-third of a patient’s plasma volume may need to be replaced. Adult plasma volume is approximately 40 mL/kg.

•  Each unit of FFP can be transfused roughly over 30-60 minutes, A slower rate or a loop diuretic can be considered if volume overload is a concern.
• In most cases, the goal is to bring INR to ≤ 1.5.
• Check the INR level 15-30 minutes after completion of the infusion and repeat the infusion until INR is ≤ 1.5; if it’s elevated, we can repeat the dose.
• The effect of fresh frozen plasma (FFP) typically lasts 6–8 hours. Keep this in mind when using FFP to reverse INR before a procedure.

Cryoprecipitate

• FFP isn’t rich in fibrinogen but can be processed in multiple ways to produce cryoprecipitate.
• Cryoprecipitate is rich in fibrinogen, Factor VIII, von Willebrand factor, and Factor XIII.
• Cryo is usually given in pools, each pool is made of 5 units or packs, and each unit is 10 to 20 mL only, which means it doesn’t carry the risk of volume overload. Each pool is typically transfused over 30 minutes.
• Cryoprecipitate is used in DIC patients who have:
  • Serious bleeԁiոg.
  • At high risk for blеeԁiոg (eg, after surgery).
  • Require invasive procedures.
• If the plasma fibriոоgen level is <100 mg/dL, we administer cryoprecipitate to increase it to >100 mg/dL.
• If the plasma fibriոоgen level is >100 mg/dL and the PТ or аPΤТ remains significantly elevated, we administer FFΡ.

• 1 unit of cryoprecipitate per 10 kg of body weight is often sufficient to raise fibrinogen by approximately 50-70 mg/dL. For a 70-kg patient with a fibrinogen level of 50 mg/dl, we will need 7 units or packs of cryo to raise the fibrinogen level to > 100 mg/dl.
• Repeat labs 30-60 minutes after all the transfusions are finished. If fibrinogen is > 100 mg/dl and the PТ or аPΤТ remains significantly elevated, we administer FFΡ.

Massive transfusion

• Massive transfusion is defined as the transfusion of 10 or more units of whole blood (WB) or packed red blood cells (PRBCs) within 24 hours, 3 or more units of PRBCs in one hour, or 4 or more blood components within 30 minutes.

• Massive transfusion may lead to dilutional coagulopathy, hypocalcemia due to citrate toxicity, hyperkalemia, and hypothermia. To address these risks, massive transfusion protocols have been developed.
• In massive transfusion, we aim to follow a 1:1:1 ratio—one unit of PRBCs, one unit of platelets, and one unit of plasma.
• Cryoprecipitate should be given if the fibrinogen level falls below 100 mg/dL, and hypocalcemia should be managed with calcium supplementation.

Transfusion reactions

• Remember that the PRBC and platelet units contain some WBC and some plasma, plasma units are acellular, and they don’t contain cells!
• Transfusion reactions may occur with any blood product and are categorized into immune and nonimmune reactions.
• Immune reactions include the hemolytic reaction, febrile Non-Hemolytic Reactions, allergic reactions, TRALI, and GVHD.

Hemolytic reactions

• Although rare today, it can still occur due to procedural errors from a major ABO incompatibility, leading to the recipient’s antibodies attacking transfused red blood cells.
• Strict ABO compatibility is required for RBC and FFP transfusions, while for platelets transfusion, ABO compatibility is preferred to reduce the risk of minor reactions or platelet refractoriness, but it is not absolutely necessary.
• Hemolytic reactions are characterized by the development of fever, chills, back or chest pain, flank pain, or pink/red urine or serum during transfusion or within 24 hours afterward.
• Stop the transfusion immediately, perform a transfusion reaction panel, and monitor the patient closely.
• The development of disseminated intravascular coagulation (DIC) and acute kidney injury (AKI) supports the diagnosis of AHTR. If confirmed, treatment is primarily supportive, and the patient should be monitored in the ICU.

Febrile Non-Hemolytic Reactions

• They are caused by reactions to donor white blood cells or cytokines present in the transfused product.
• They are characterized by an isolated fever above 38°C or 100.4℉, chills, or rigors during a transfusion or within 4 hours afterward.
• Primarily occurs with RBC and platelet transfusions and is rare with plasma transfusions, as plasma is acellular.
• To reduce the risk of febrile reactions, RBCs and platelets can undergo leukocyte reduction, resulting in leukocyte-depleted RBCs or platelets.
• Stop the transfusion immediately and perform a transfusion reaction panel.
• Acetaminophen can be administered to reduce fever.
• If the transfusion reaction panel is negative and the fever resolves, the transfusion can be resumed with a new unit.
• Consider using leukocyte-depleted units if available, and discard the unit that led to the reaction.
• It’s worth noting that there is no strong evidence to support premedication with acetaminophen or antihistamines.

Allergic Reactions

• This happens due to hypersensitivity to proteins in donor plasma.
• Common with platelets and FFP transfusions due to plasma proteins but less with PRBCs transfusion.
• It is characterized by the development of pruritus, hives, urticaria, or localized angioedema—without wheezing, shortness of breath, systemic angioedema, or hemodynamic instability.
• This reaction may occur during, at the end of, or shortly after a transfusion.
• Stop the transfusion immediately and administer diphenhydramine, which usually resolves symptoms quickly. If symptoms persist, a second dose of diphenhydramine may be given.
• To reduce the risk of allergic reactions, the platelets and RBC can be washed from the plasma, so-called washed RBCs or platelets.
• Once symptoms have subsided, the transfusion may be resumed with the same unit, as the remainder can be used safely, unlike with other types of transfusion reactions.

Anaphylactic reactions

• Typically occurs within seconds to minutes of starting the transfusion with rapid onset of shock, hypotension, angioedema, respiratory distress, and/or wheezing.
• Immediately stop the transfusion and administer epinephrine along with antihistamines and other supportive treatments as needed.
• Evaluate these patients for IgA deficiency, as IgA-deficient individuals may have antibodies that can trigger severe reactions.
• For future transfusions, consider using IgA-deficient blood products or washed red blood cells to minimize the risk of recurrence.
• Premedication with antihistamines and corticosteroids may also be considered, though its effectiveness varies.

TRALI (Transfusion-related acute lung injury)

• It may happen due to donor antibodies reacting with recipient leukocytes, causing inflammation and capillary leak in the lungs.
• It’s more likely to happen with plasma-containing products (FFP, platelets, and to some extent cryo) due to the risk of donor antibodies against recipient leukocytes.
• TACO (Transfusion-associated circulatory overload) is a nonimmune reaction caused by fluid overload from the transfusion, resulting in pulmonary edema.
• Both TRALI and TACO can present with similar symptoms, including shortness of breath, hypoxia, and bilateral infiltrates on a chest X-ray. However, TRALI tends to cause more severe hypoxia and respiratory distress.
• Stop transfusion, administer IV loop diuretics, and provide supplemental oxygen to correct hypoxia, patients likely will require noninvasive positive pressure ventilation or mechanical ventilation. If it’s TACO, the patient responds quickly to diuretics, while TRALI does not and requires supportive care similar to acute respiratory distress syndrome (ARDS).
• An individual with previous TRALI can receive blood products from other donors without restrictions but should not receive any remaining untransfused portion of the implicated product or any other products from the implicated donor.

Graft versus host disease (GVHD)

GVHD transfusion reaction is rare and happens in immunocompromised patients when the donor lymphocyte identifies the recipient’s tissues as foreign and attacks them. To reduce this risk, PRBC or platelets can be irradiated to destroy the donor WBC including lymphocytes before transfusion to immunocompromised patients.

To wrap up:

• Leukocyte-reduced RBC/platelets are used to reduce the risk of febrile nonhemolytic transfusion reactions.
• Washed RBC/platelets are used to reduce the risk of allergic reactions.
• Irradiated RBC/platelets are used in immunocompromised patients to reduce the risk of GVHD.

Eight EKG patterns we can’t afford to miss! These patterns, in the right clinical context, are suggestive of acute coronary occlusion and require immediate reperfusion therapy without any delay!