UBP 3.8 (Long Form): Renal – CRF & Kidney Transplant Flashcards
Secondary Subject -- Preoperative Hypertension/Chronic Hyperkalemia/ Pulmonary Edema/Uremic Thrombocytopathia
Intra-Operative Management:
Assume you are proceeding with general anesthesia.
Is invasive monitoring indicated in this case?
- (A 42-year-old, 84 kg, man is brought to the OR for nephrectomy and transplantation of a cadaveric kidney harvested 16 hours ago.*
- PMHx: The patient has chronic renal failure secondary to uncontrolled hypertension. He has been on hemodialysis for 8 years, with his most recent dialysis occurring 24 hours ago. He was diagnosed with hypertension 24 years ago. Additional medical history includes an episode of acute pulmonary edema.*
- Meds: Nifedipine, lisinopril, ranitidine, OTC antacids*
- Allergies: PCN, Codeine*
- PE: Vital signs: P = 95, BP = 195/110 mmHg, RR = 22, T = 37 °C*
- General: patient is anxious and tearful*
- Airway: Mallampati II, TMD > 6 cm, full neck ROM*
- Lungs: decreased breath sounds bilaterally*
- Extremities: AV fistula in left forearm; 20-gauge IV in right hand*
- CXR: cardiomegaly, small bilateral pleural effusions*
- EKG: LVH, non-specific ST changes*
- Labs: Hgb 8.0 gm/dL, Na+ 134 mEq/L, K+ 5.2 mEq/L, BUN 49 mg/dL)*
This patient’s uncertain volume status and poorly controlled preoperative hypertension place him at increased risk of hemodynamic instability during induction, laryngoscopy, and unclamping of the iliac vessels following graft placement.
Therefore, i believe placing a CVP catheter and arterial line would be beneficial in rapidly identifying and treating hemodynamic changes that place the patient at increased risk for complications such as myocardial ischemia/infarction, cerebrovascular events, and delayed or compromised graft function.
Additionally, optimization of the patient’s intravascular volume may reduce the incidence of post-operative acute tubular necrosis and promote early onset of graft function;
CVP monitoring may help to facilitate this goal while, at the same time, avoiding fluid overload.
Finally, if additional history or the physical exam identified congestive heart failure, significant coronary artery disease, valvular heart disease, left ventricular dysfunction, or severe chronic obstructive pulmonary disease, I would consider placing a pulmonary artery catheter.
Intra-Operative Management:
How will you induce this patient?
- (A 42-year-old, 84 kg, man is brought to the OR for nephrectomy and transplantation of a cadaveric kidney harvested 16 hours ago.*
- PMHx: The patient has chronic renal failure secondary to uncontrolled hypertension. He has been on hemodialysis for 8 years, with his most recent dialysis occurring 24 hours ago. He was diagnosed with hypertension 24 years ago. Additional medical history includes an episode of acute pulmonary edema.*
- Meds: Nifedipine, lisinopril, ranitidine, OTC antacids*
- Allergies: PCN, Codeine*
- PE: Vital signs: P = 95, BP = 195/110 mmHg, RR = 22, T = 37 °C*
- General: patient is anxious and tearful*
- Airway: Mallampati II, TMD > 6 cm, full neck ROM*
- Lungs: decreased breath sounds bilaterally*
- Extremities: AV fistula in left forearm; 20-gauge IV in right hand*
- CXR: cardiomegaly, small bilateral pleural effusions*
- EKG: LVH, non-specific ST changes*
- Labs: Hgb 8.0 gm/dL, Na+ 134 mEq/L, K+ 5.2 mEq/L, BUN 49 mg/dL)*
My goal during induction is to safely secure airway while avoiding hypotension or hypertension in this patient with poorly controlled hypertension, who is potentially volume contracted and more likely to exhibit an exaggerated response to laryngoscopy.
Therefore, as long as there was not significant risk of aspiration (i.e. uremic gastroparesis), I would perform a slow controlled induction after placing the appropriate monitors, ensuring adequate B-blockade and hydration, and administering intravenous lidocaine to further attenuate a sympathetic response to laryngoscopy.
Following intubation, I would maintain general anesthesia using a volatile agent, a short acting opioid (consider using opioids without active metabolites that depend on renal excretion), and a muscle relaxant (mivacurium, atracurium, cisatracurium do not depend on renal excretion) in order to provide optimal operating conditions.
Intra-Operative Management:
Would sevoflurane be a good choice for a volatile agent?
- (A 42-year-old, 84 kg, man is brought to the OR for nephrectomy and transplantation of a cadaveric kidney harvested 16 hours ago.*
- PMHx: The patient has chronic renal failure secondary to uncontrolled hypertension. He has been on hemodialysis for 8 years, with his most recent dialysis occurring 24 hours ago. He was diagnosed with hypertension 24 years ago. Additional medical history includes an episode of acute pulmonary edema.*
- Meds: Nifedipine, lisinopril, ranitidine, OTC antacids*
- Allergies: PCN, Codeine*
- PE: Vital signs: P = 95, BP = 195/110 mmHg, RR = 22, T = 37 °C*
- General: patient is anxious and tearful*
- Airway: Mallampati II, TMD > 6 cm, full neck ROM*
- Lungs: decreased breath sounds bilaterally*
- Extremities: AV fistula in left forearm; 20-gauge IV in right hand*
- CXR: cardiomegaly, small bilateral pleural effusions*
- EKG: LVH, non-specific ST changes*
- Labs: Hgb 8.0 gm/dL, Na+ 134 mEq/L, K+ 5.2 mEq/L, BUN 49 mg/dL)*
Given the potential risk of nephrotoxicity with the use of sevoflurane, I don’t believe it would be a good choice for kidney transplant surgery.
The concern of nephrotoxicity stems from the fact that –
- sevoflurane metabolism leads to the formation of potentially nephrotoxic levels of inorganic fluoride (>50 umol/L), and that
- degradation by sodium or barium hydroxide (barium hydroxide > soda lime) can lead to the production of compound A, which has been associated with renal toxicity in animals.
However, despite these theoretical or potential risks, sevoflurane has been successfully used for kidney transplant surgery.
If using sevoflurane became necessary for some reason, I would –
- minimize the length of patient exposure to the agent,
- ensure gas flow rates of at least 2 L per minute (>1 L per minute is ok for cases lasting less than 1 hour), and
- make sure my carbon dioxide absorbent is not desiccated (consideration could also be given to using Amsorb, which contains calcium hydroxide & calcium chloride, and results in less degradation of volatile agents).
Intra-Operative Management:
How will you manage fluids during this case?
Which fluids would you use for replacement?
- (A 42-year-old, 84 kg, man is brought to the OR for nephrectomy and transplantation of a cadaveric kidney harvested 16 hours ago.*
- PMHx: The patient has chronic renal failure secondary to uncontrolled hypertension. He has been on hemodialysis for 8 years, with his most recent dialysis occurring 24 hours ago. He was diagnosed with hypertension 24 years ago. Additional medical history includes an episode of acute pulmonary edema.*
- Meds: Nifedipine, lisinopril, ranitidine, OTC antacids*
- Allergies: PCN, Codeine*
- PE: Vital signs: P = 95, BP = 195/110 mmHg, RR = 22, T = 37 °C*
- General: patient is anxious and tearful*
- Airway: Mallampati II, TMD > 6 cm, full neck ROM*
- Lungs: decreased breath sounds bilaterally*
- Extremities: AV fistula in left forearm; 20-gauge IV in right hand*
- CXR: cardiomegaly, small bilateral pleural effusions*
- EKG: LVH, non-specific ST changes*
- Labs: Hgb 8.0 gm/dL, Na+ 134 mEq/L, K+ 5.2 mEq/L, BUN 49 mg/dL)*
I would use central venous pressure monitoring (or the PAC, if present) and vigilance to optimize the patient’s volume status and maintain renal blood flow, which is important in reducing the incidence of post-operative acute tubular necrosis and promoting early onset of graft function.
Assuming the patient was normovolemic at the start of the case, I would replace blood loss with an isotonic solution, such as normal saline or Plasma-Lyte, at a ratio of 3:1, avoiding potassium containing solutions, such as Ringer lactate, that could exacerbate intraoperative hyperkalemia.
If rapid resuscitation of intravascular volume became necessary, as may occur with unclamping of the iliac vessels and perfusion of the newly transplanted graft, I would consider using a low-molecular-weight hydroxyethyl starch (coagulopathy is unusual when < 33 ml/kg are administered).
If the administration of blood became necessary, I would transfuse cytomegalovirus-negative packed red blood cells.
Intra-Operative Management:
Are there any drugs you would give prior to clamping of the iliac vessels?
- (A 42-year-old, 84 kg, man is brought to the OR for nephrectomy and transplantation of a cadaveric kidney harvested 16 hours ago.*
- PMHx: The patient has chronic renal failure secondary to uncontrolled hypertension. He has been on hemodialysis for 8 years, with his most recent dialysis occurring 24 hours ago. He was diagnosed with hypertension 24 years ago. Additional medical history includes an episode of acute pulmonary edema.*
- Meds: Nifedipine, lisinopril, ranitidine, OTC antacids*
- Allergies: PCN, Codeine*
- PE: Vital signs: P = 95, BP = 195/110 mmHg, RR = 22, T = 37 °C*
- General: patient is anxious and tearful*
- Airway: Mallampati II, TMD > 6 cm, full neck ROM*
- Lungs: decreased breath sounds bilaterally*
- Extremities: AV fistula in left forearm; 20-gauge IV in right hand*
- CXR: cardiomegaly, small bilateral pleural effusions*
- EKG: LVH, non-specific ST changes*
- Labs: Hgb 8.0 gm/dL, Na+ 134 mEq/L, K+ 5.2 mEq/L, BUN 49 mg/dL)*
Usually heparin is administered prior to clamping the iliac vessels to prevent clotting.
Just prior to revascularization, a calcium channel blocker (verapamil) or papaverine is often injected into the arterial circulation of the graft to prevent arterial vasospasm and/or reperfusion injury.
Finally, mannitol and/or furosemide are given following reperfusion to induce diuresis.
Mannitol has the added advantage of acting as a free radical scavenger.
Intra-Operative Management:
After unclamping, his blood pressure falls to 61/40 mmHg. What do you think is going on?
- (A 42-year-old, 84 kg, man is brought to the OR for nephrectomy and transplantation of a cadaveric kidney harvested 16 hours ago.*
- PMHx: The patient has chronic renal failure secondary to uncontrolled hypertension. He has been on hemodialysis for 8 years, with his most recent dialysis occurring 24 hours ago. He was diagnosed with hypertension 24 years ago. Additional medical history includes an episode of acute pulmonary edema.*
- Meds: Nifedipine, lisinopril, ranitidine, OTC antacids*
- Allergies: PCN, Codeine*
- PE: Vital signs: P = 95, BP = 195/110 mmHg, RR = 22, T = 37 °C*
- General: patient is anxious and tearful*
- Airway: Mallampati II, TMD > 6 cm, full neck ROM*
- Lungs: decreased breath sounds bilaterally*
- Extremities: AV fistula in left forearm; 20-gauge IV in right hand*
- CXR: cardiomegaly, small bilateral pleural effusions*
- EKG: LVH, non-specific ST changes*
- Labs: Hgb 8.0 gm/dL, Na+ 134 mEq/L, K+ 5.2 mEq/L, BUN 49 mg/dL)*
Hypotension immediately following unclamping is most likely secondary to the washout of vasoactive substances from previously ischemic tissues and the acute increases of up to 300 ml to the intravascular space.
However, I would also consider –
- congestive heart failure,
- secondary to fluid overload or cardiac ischemia;
- dysrhythmia,
- secondary to cardiac ischemia or acute hyperkalemia;
- anaphylaxis,
- secondary to antibiotics, thymoglobulin, etc.;
- blood loss;
- tension pneumothorax
- (possibly secondary to central line placement);
- anesthetic overdose;
- hypoxia; and
- monitor error.
In response, I would –
- ensure adequate oxygenation and ventilation;
- auscultate the lungs;
- check the EKG for dysrhythmia;
- check the CVP and PAC pressures (if available);
- consider transesophageal echocardiography, if the etiology of the hypotension remains unclear;
- inspect the surgical field for bleeding;
- check serum electrolytes (i.e. hyperkalemia, hyponatremia); and
- prepare to treat with fluids, inotropes, and vasopressors, as indicated.
Intra-Operative Management:
You see peaked T waves on the EKG.
What are you going to do?
- (A 42-year-old, 84 kg, man is brought to the OR for nephrectomy and transplantation of a cadaveric kidney harvested 16 hours ago.*
- PMHx: The patient has chronic renal failure secondary to uncontrolled hypertension. He has been on hemodialysis for 8 years, with his most recent dialysis occurring 24 hours ago. He was diagnosed with hypertension 24 years ago. Additional medical history includes an episode of acute pulmonary edema.*
- Meds: Nifedipine, lisinopril, ranitidine, OTC antacids*
- Allergies: PCN, Codeine*
- PE: Vital signs: P = 95, BP = 195/110 mmHg, RR = 22, T = 37 °C*
- General: patient is anxious and tearful*
- Airway: Mallampati II, TMD > 6 cm, full neck ROM*
- Lungs: decreased breath sounds bilaterally*
- Extremities: AV fistula in left forearm; 20-gauge IV in right hand*
- CXR: cardiomegaly, small bilateral pleural effusions*
- EKG: LVH, non-specific ST changes*
- Labs: Hgb 8.0 gm/dL, Na+ 134 mEq/L, K+ 5.2 mEq/L, BUN 49 mg/dL)*
Peaked T waves on the EKG are consistent with significant hyperkalemia, which may occur with perfusion of the newly transplanted kidney and subsequent washout of potassium-containing preservative solution into the systemic circulation.
Therefore, I would order a plasma potassium level, notify the surgeon, and initiate treatment, with the goals of:
- eliminating any factors that may exacerbate hyperkalemic cardiotoxicity, such as acidosis, hyponatremia, and hypocalcemia (all of which occur in the presence of impaired renal function);
- depressing cardiac membrane hyperexcitability; and
- reducing extracellular fluid potassium, by either shifting it into cells or removing it from the body.
I would also ensure immediate access to a cardiac defibrillator and prepare to treat cardiovascular dysrhythmias and instability as necessary.
Intra-Operative Management:
What are the characteristic EKG changes associated with hyperkalemia?
- (A 42-year-old, 84 kg, man is brought to the OR for nephrectomy and transplantation of a cadaveric kidney harvested 16 hours ago.*
- PMHx: The patient has chronic renal failure secondary to uncontrolled hypertension. He has been on hemodialysis for 8 years, with his most recent dialysis occurring 24 hours ago. He was diagnosed with hypertension 24 years ago. Additional medical history includes an episode of acute pulmonary edema.*
- Meds: Nifedipine, lisinopril, ranitidine, OTC antacids*
- Allergies: PCN, Codeine*
- PE: Vital signs: P = 95, BP = 195/110 mmHg, RR = 22, T = 37 °C*
- General: patient is anxious and tearful*
- Airway: Mallampati II, TMD > 6 cm, full neck ROM*
- Lungs: decreased breath sounds bilaterally*
- Extremities: AV fistula in left forearm; 20-gauge IV in right hand*
- CXR: cardiomegaly, small bilateral pleural effusions*
- EKG: LVH, non-specific ST changes*
- Labs: Hgb 8.0 gm/dL, Na+ 134 mEq/L, K+ 5.2 mEq/L, BUN 49 mg/dL)*
EKG signs associated with hyperkalemia, (usually when plasma potassium levels exceed 6 mEq/L) characteristically progress
- from peaked T waves,
- to prolongation of the PR interval,
- to decreasing amplitude,
- to loss of the P wave,
- to widening of the QRS complex (representing the loss of atrial activity),
- to a sine wave pattern, and finally,
- to ventricular fibrillation and asystole (usually occurring at levels around 8-9 mEq/L).
Intra-Operative Management:
How would you treat this hyperkalemic patient with associated electrocardiographic changes?
- (A 42-year-old, 84 kg, man is brought to the OR for nephrectomy and transplantation of a cadaveric kidney harvested 16 hours ago.*
- PMHx: The patient has chronic renal failure secondary to uncontrolled hypertension. He has been on hemodialysis for 8 years, with his most recent dialysis occurring 24 hours ago. He was diagnosed with hypertension 24 years ago. Additional medical history includes an episode of acute pulmonary edema.*
- Meds: Nifedipine, lisinopril, ranitidine, OTC antacids*
- Allergies: PCN, Codeine*
- PE: Vital signs: P = 95, BP = 195/110 mmHg, RR = 22, T = 37 °C*
- General: patient is anxious and tearful*
- Airway: Mallampati II, TMD > 6 cm, full neck ROM*
- Lungs: decreased breath sounds bilaterally*
- Extremities: AV fistula in left forearm; 20-gauge IV in right hand*
- CXR: cardiomegaly, small bilateral pleural effusions*
- EKG: LVH, non-specific ST changes*
- Labs: Hgb 8.0 gm/dL, Na+ 134 mEq/L, K+ 5.2 mEq/L, BUN 49 mg/dL)*
Given the presence of EKG changes, I would:
- give calcium chloride or calcium gluconate to depress cardiac membrane excitability (immediate effect);
- ensure immediate access to a cardiac defibrillator and prepare to treat cardiovascular dysrhythmias and instability as necessary;
- attempt to correct any factors that may exacerbate hyperkalemic cardiotoxicity, such as acidosis, hyponatremia, and hypocalcemia;
- attempt to shift extracellular potassium into cells by administering insulin and glucose (effective in 10-20 minutes), B2-adrenergic drugs (albuterol, salbutamol), and possibly sodium bicarbonate (although the latter is not considered very effective);
- hyperventilate the patient to promote alkalosis and subsequent intracellular movement of potassium; and
- consider hemodialysis, if temporizing measures are insufficient.
Post-Operative Management:
After extubation in the operating room, the patient develops rapid and labored breathing. Auscultation of the lungs reveals diffuse rales. Will you reintubate?
- (A 42-year-old, 84 kg, man is brought to the OR for nephrectomy and transplantation of a cadaveric kidney harvested 16 hours ago.*
- PMHx: The patient has chronic renal failure secondary to uncontrolled hypertension. He has been on hemodialysis for 8 years, with his most recent dialysis occurring 24 hours ago. He was diagnosed with hypertension 24 years ago. Additional medical history includes an episode of acute pulmonary edema.*
- Meds: Nifedipine, lisinopril, ranitidine, OTC antacids*
- Allergies: PCN, Codeine*
- PE: Vital signs: P = 95, BP = 195/110 mmHg, RR = 22, T = 37 °C*
- General: patient is anxious and tearful*
- Airway: Mallampati II, TMD > 6 cm, full neck ROM*
- Lungs: decreased breath sounds bilaterally*
- Extremities: AV fistula in left forearm; 20-gauge IV in right hand*
- CXR: cardiomegaly, small bilateral pleural effusions*
- EKG: LVH, non-specific ST changes*
- Labs: Hgb 8.0 gm/dL, Na+ 134 mEq/L, K+ 5.2 mEq/L, BUN 49 mg/dL)*
I would re-intubate at any point that delaying a definitive airway for further evaluation would place the patient at an unacceptable amount of risk.
However, if the patient were stable enough to allow further investigation, I would provide supplemental oxygen and assess oxygenation and ventilation by carefully auscultating all lung fields, evaluating the patient’s oxygen saturation and inspiratory effort, and obtaining an ABG.
Next, I would evaluate his cardiovascular function by checking the CVP, PAC (if present), EKG, and arterial blood pressure; and by ordering a chest x-ray and, possibly, an echocardiogram.
Additionally, I would check the patient’s electrolytes and review all medications, giving careful consideration to whether renal excretion played a significant role in the elimination of the parent compounds and/or their active metabolites.
Finally, depending on my findings, I would consider – diuretics, hemodialysis, bronchodilators, inotropes, afterload reducing agents, and re-intubation.
Post-Operative Management:
The chest x-ray suggests bilateral pulmonary edema and his oxygen saturation is 84%.
How might mechanical ventilation prove beneficial?
- (A 42-year-old, 84 kg, man is brought to the OR for nephrectomy and transplantation of a cadaveric kidney harvested 16 hours ago.*
- PMHx: The patient has chronic renal failure secondary to uncontrolled hypertension. He has been on hemodialysis for 8 years, with his most recent dialysis occurring 24 hours ago. He was diagnosed with hypertension 24 years ago. Additional medical history includes an episode of acute pulmonary edema.*
- Meds: Nifedipine, lisinopril, ranitidine, OTC antacids*
- Allergies: PCN, Codeine*
- PE: Vital signs: P = 95, BP = 195/110 mmHg, RR = 22, T = 37 °C*
- General: patient is anxious and tearful*
- Airway: Mallampati II, TMD > 6 cm, full neck ROM*
- Lungs: decreased breath sounds bilaterally*
- Extremities: AV fistula in left forearm; 20-gauge IV in right hand*
- CXR: cardiomegaly, small bilateral pleural effusions*
- EKG: LVH, non-specific ST changes*
- Labs: Hgb 8.0 gm/dL, Na+ 134 mEq/L, K+ 5.2 mEq/L, BUN 49 mg/dL)*
Mechanical ventilation, and more specifically PEEP, may prove beneficial for patients with pulmonary edema, secondary to a positive-pressure-induced redistribution of alveolar fluid into areas that are less involved in gas exchange, which leads to improved oxygenation.
However, in the presence of left ventricular dysfunction, positive ventilation and PEEP must be applied with caution to prevent worsening cardiac function secondary to decreased preload
(positive intrathoracic pressure decreases blood return to the heart through the inferior vena cava).
It is also important to avoid over-inflation of alveoli, which can result in barotrauma, increased capillary permeability, and potentially worsening pulmonary edema.
Post-Operative Management:
If you didn’t place a pulmonary artery catheter for the case, would you place one now?
- (A 42-year-old, 84 kg, man is brought to the OR for nephrectomy and transplantation of a cadaveric kidney harvested 16 hours ago.*
- PMHx: The patient has chronic renal failure secondary to uncontrolled hypertension. He has been on hemodialysis for 8 years, with his most recent dialysis occurring 24 hours ago. He was diagnosed with hypertension 24 years ago. Additional medical history includes an episode of acute pulmonary edema.*
- Meds: Nifedipine, lisinopril, ranitidine, OTC antacids*
- Allergies: PCN, Codeine*
- PE: Vital signs: P = 95, BP = 195/110 mmHg, RR = 22, T = 37 °C*
- General: patient is anxious and tearful*
- Airway: Mallampati II, TMD > 6 cm, full neck ROM*
- Lungs: decreased breath sounds bilaterally*
- Extremities: AV fistula in left forearm; 20-gauge IV in right hand*
- CXR: cardiomegaly, small bilateral pleural effusions*
- EKG: LVH, non-specific ST changes*
- Labs: Hgb 8.0 gm/dL, Na+ 134 mEq/L, K+ 5.2 mEq/L, BUN 49 mg/dL)*
Given the presence of significant pulmonary edema, potentially compromised cardiac function (normal cardiac function is required for CVP to accurately reflect left heart filling pressures), and the importance of maintaining adequate renal blood flow in this post-transplant patient,
I would certainly consider placing a pulmonary artery catheter to aid in fluid management, assess cardiac function, and help differentiate cardiac and noncardiac causes of his pulmonary edema.
Post-Operative Management:
One hour post-operatively, the patient is oozing from the surgical incision.
What do you think is going on?
- (A 42-year-old, 84 kg, man is brought to the OR for nephrectomy and transplantation of a cadaveric kidney harvested 16 hours ago.*
- PMHx: The patient has chronic renal failure secondary to uncontrolled hypertension. He has been on hemodialysis for 8 years, with his most recent dialysis occurring 24 hours ago. He was diagnosed with hypertension 24 years ago. Additional medical history includes an episode of acute pulmonary edema.*
- Meds: Nifedipine, lisinopril, ranitidine, OTC antacids*
- Allergies: PCN, Codeine*
- PE: Vital signs: P = 95, BP = 195/110 mmHg, RR = 22, T = 37 °C*
- General: patient is anxious and tearful*
- Airway: Mallampati II, TMD > 6 cm, full neck ROM*
- Lungs: decreased breath sounds bilaterally*
- Extremities: AV fistula in left forearm; 20-gauge IV in right hand*
- CXR: cardiomegaly, small bilateral pleural effusions*
- EKG: LVH, non-specific ST changes*
- Labs: Hgb 8.0 gm/dL, Na+ 134 mEq/L, K+ 5.2 mEq/L, BUN 49 mg/dL)*
The most common cause of post-operative coagulopathy is platelet dysfunction, which may result secondary to –
- uremia (interferes with vWF formation and release),
- hypothermia (affects the morphology and function of platelets),
- drug effect, or
- severe anemia (with decreased viscosity, the platelets tend to travel in the center of the blood column, instead of near the endothelial surface).
However, I would also consider other causes of coagulopathy such as –
- residual heparin effect,
- inadequate surgical hemostasis,
- metabolic acidosis (interferes with the generation of thrombin),
- thrombocytopenia, and
- DIC.
Therefore, I would check a platelet count, PT, PTT, INR, CBC, fibrinogen level, and fibrin degradation products.
TEG analysis may also prove helpful, if available.
Post-Operative Management:
What is the cause of uremic thrombocytopathia?
- (A 42-year-old, 84 kg, man is brought to the OR for nephrectomy and transplantation of a cadaveric kidney harvested 16 hours ago.*
- PMHx: The patient has chronic renal failure secondary to uncontrolled hypertension. He has been on hemodialysis for 8 years, with his most recent dialysis occurring 24 hours ago. He was diagnosed with hypertension 24 years ago. Additional medical history includes an episode of acute pulmonary edema.*
- Meds: Nifedipine, lisinopril, ranitidine, OTC antacids*
- Allergies: PCN, Codeine*
- PE: Vital signs: P = 95, BP = 195/110 mmHg, RR = 22, T = 37 °C*
- General: patient is anxious and tearful*
- Airway: Mallampati II, TMD > 6 cm, full neck ROM*
- Lungs: decreased breath sounds bilaterally*
- Extremities: AV fistula in left forearm; 20-gauge IV in right hand*
- CXR: cardiomegaly, small bilateral pleural effusions*
- EKG: LVH, non-specific ST changes*
- Labs: Hgb 8.0 gm/dL, Na+ 134 mEq/L, K+ 5.2 mEq/L, BUN 49 mg/dL)*
The mechanisms by which uremia contributes to thrombocytopathia include:
- decreased von Willebrand factor (vWF) formation and release secondary to the accumulation of various metabolites,
- increased synthesis of nitric oxide and prostacyclin, which have platelet inhibitory effects, and
- uremia-induced anemia, which contributes to decreased viscosity with a subsequent decrease in platelet interaction with endothelial surfaces.
Patients with chronic renal failure may also be more susceptible to coagulopathy because they tend to have reduced levels of factor V and the vitamin K-dependent factors (II, VII, IX, X).
Post-Operative Management:
How do you treat uremic thrombocytopathia?
- (A 42-year-old, 84 kg, man is brought to the OR for nephrectomy and transplantation of a cadaveric kidney harvested 16 hours ago.*
- PMHx: The patient has chronic renal failure secondary to uncontrolled hypertension. He has been on hemodialysis for 8 years, with his most recent dialysis occurring 24 hours ago. He was diagnosed with hypertension 24 years ago. Additional medical history includes an episode of acute pulmonary edema.*
- Meds: Nifedipine, lisinopril, ranitidine, OTC antacids*
- Allergies: PCN, Codeine*
- PE: Vital signs: P = 95, BP = 195/110 mmHg, RR = 22, T = 37 °C*
- General: patient is anxious and tearful*
- Airway: Mallampati II, TMD > 6 cm, full neck ROM*
- Lungs: decreased breath sounds bilaterally*
- Extremities: AV fistula in left forearm; 20-gauge IV in right hand*
- CXR: cardiomegaly, small bilateral pleural effusions*
- EKG: LVH, non-specific ST changes*
- Labs: Hgb 8.0 gm/dL, Na+ 134 mEq/L, K+ 5.2 mEq/L, BUN 49 mg/dL)*
The treatment options for uremic thrombocytopathia include:
- desmopressin (DDAVP) to increase the release of vWF;
- erythropoeitin, which may exert its effect by correcting anemia;
- conjugated estrogens, which may reduce nitric oxide formation;
- cryoprecipitate, which contains vWF;
- platelets; and
- hemodialysis to remove uremic acid.
–
The fastest and most effective treatment is hemodialysis, which eliminates the uremic acid and quickly restores adequate platelet function.
If hemodialysis were ineffective in correcting a clinically significant and life-threatening thrombocytyopathic coagulopathy, I would consider a platelet transfusion.
