Anesthetic Approach To Chronic Renal Failure Patients

Introduction:

Despite different causes of CRF , the common presentation is progressive irreversible loss of functioning nephrons, with an associated decrease in the GFR

Uremia occurs when less than 10% of nephrons are functioning

Preoperative Evaluation Of CRF Patients

This include:

# Characteristic changes of CRF

# Concomitant drug therapy

# Estimation of blood volume

# Considerations regarding vital signs, and atrial filling pressure

# Diabetes mellitus

Characteristic Changes of CRF

1- metabolic changes , and electrolytes imbalance.

2- Hematologic.

3- Cardiovascular.

4- Respiratory.

5- Endocrine.

6- GIT.

7- Neurologic.

I- Metabolic, Changes

Metabolic Acidosis:

The Kidney normally excretes 50 to 100 mEq. Of H+ ion per day, reflecting metabolism of dietary protein. High anion gap metabolic acidosis with PH < 7.3 is due to failure to excrete non volatile acid. This depress neuromuscular response, and stimulate compensatory hyperventilation.

Hypoalbuminimia:

Rapid loss of tissue protein, anorexia, protein dietary restriction, dialysis specially peritoneal are contributory factors to development of hypoprotieneamia.

Electrolytes Imbalance

• Hyperkalemia

• Hypermagnesemia

• Hyperphosphatemia

• Hypocalcemia

• Hyponitremia

Hyperkalemia

Hyperkalemia develops rapidly even with high clearance > 5ml/min. When high K+ load is suspected (trauma, heamolysis, infection, and K+ administration).

ECG changes (peaked T wave, prolonged P-R, heart block, and ventricular fibrillation) remain the best guide to the need of treatment.

Hyperphosphatemia, And Hypocalcemia

• Hypocalcemia occurs when the GFR decline to the level of development of Hyperphosphatemia, leading to reciprocal change in plasma ca++ .

• Hypocalcemia stimulate the release of parathyroid hormone, with subsequent (renal osteodystrophy), and liability of pathological fracture.

• The possible causes of hypo ca++ is its decreased absorption from the GIT secondary to decrease renal synthesis of 1,25 dihydroxycholecalciferol, deposition of ca++ into bone secondary to Hyperphosphatemia, and resistance to parathyroid hormone.

Hypermagnesemia

• Hypermagnesemia specially develops when antacids are used.

• CNS depression up to coma, hypotension, hypoventilation, and potentiation of all types muscle relaxants.

Hyponitremia

Plasma Na+ conc. Is usually normal in CRF because osmoreceptors mechanism is functioning, however Hyponitremia may develop due to dilution (excess water intake), together with hypoalbuminimia result in ECF overload

 

II- Hematologic Changes

A- anemia:

Either due to.

• I- Bone marrow depression.

# Decreased Erythropoietin production.

# Recent infection.

• II- Blood loss.

This is an addional factor specially from GIT.

B- Coagulopathy

• Despite normal PT, PTT, and platelet count uremic patients have abnormally prolonged bleeding time.

• This is due to defective platelet aggregation, adhesiveness, and decreased platelet factor III (von-willebrand).

• The most important sites of bleeding are GIT, epistaxis, pericardium, and subdura.

III- Cardiovascular

• I- Circulatory:

• The C.O.P. has to increase to compensate for anemia.

• Intravascular Vo. expansion, abnormal Renin Angiotensin, and Aldosterone result in systemic hypertension.

• Lt ventricular hypertrophy then become a manifestation of CRF.

LVH + salt & water retention

M.I. & Stroke

LVH + Salt & water retention + AV fistula + M.I

CHF and pulmonary edema

II- Cardiac:• Conduction blocks are common due to ca++

deposition in the conducting system.• Arrhythmias are common, in part related to the

metabolic abnormalities.III-Pericardium:• Pericarditis may be a symptomatic or with chest

pain.• Pericardial effusion, related to circulating toxins

may lead to cardiac temponad.VI- Vascular: • Accelerated coronary, and peripheral vascular

disease.

IV- Pulmonary

• Un less on treatment or dialysis patients depends on hyperventilation to compensate for acidosis.

• Interstitial pulmonary edema widening the alveolar arterial oxygen gradient predispose to hypoxemia.

• Pulmonary edema develop due to increased permeability of alveolar capillary membrane, even with normal PCP giving butterfly wing on chest X ray.

V- Endocrine

• Increased peptide proteins of insulin, parathyroid, glucagons, LH, and prolactine are found in CRF.

• That is why for diabetic patient recently develop RF glucose tolerance is improved, but later insulin resistance occur during the course of RF.

• Pathological fractures are a feature of hyperparathyroidism.

• Hypertriglyceridmia accelerate the process of arteriosclerosis.

VI- Gastrointestinal

• Anorexia, nausea, and vomiting are due to azotemia.

• Increased HCL with peptic ulceration is found in 10-30% of patients , with GIT hemorrhage.

• Neuropathy delayed gastric empty time with increased liability of aspiration.

• Hepatitis B & C are common findings in patients with CRF.

VII- Neurologic

• There are three causes of Neurologic manifestation.• 1- Azotemia leading to lethargy, confusion,

seizures, and coma.• 2- Brain edema caused by acute hypertension.• 3- DM causes autonomic neuropathy, but sensory

and motor nerves may be involved (median, and common peroneal nerves).

• * Attention to autonomic neuropathy because it attenuate compensatory mechanisms to change in blood volume or PPV.

Concomitant Drug Therapy

• Treatment Of Blood Disorders:

Erythropoietin:

• This drug is capable to to reduce the need of repeated blood transfusion. It is administrated till Hematocrit reach 30-33%.

• Owing to it’s capability to lower plasma histamine, it is useful in treatment pruritus of end stage renal failure, but it exacerbates hypertension.

• Also it is effective in treatment of coagulopathies.

Other Treatment Of Coagulopathies

• 1-Desmopressin:• It is a nonvasoconstrictor analogue of vasopressin (0.3-0.4

mg/Kg/min. over 30 min.) of IV infusion decreases BT with peak effect 1-4, and last 4-8 hr.

• An alternative is the use of cryopprecipitate.• 2- Estrogen:• Has a more prolonged beneficial effect (14 day).• 3-Dialysis:• The least effective to improve coagulation in uremic

bleeding.

Treatment Of Hyperkalemia1- Dialysis.

2- Glucose insulin infusion.

3- Calcium is the effective physiological antidote of hyperkalemic side effects on the myocardium.

Acidosis:

• NaHCO3 infusion started when the PH = 7.15 with attention toward calcium level not to drop.

Hypertension:

• # If it is due to Vo. Over load, dialysis is effective.

• # If it is due to Renin system activation, dialysis has no role.

• At the same time AC inhibitors, and ca++ channel blockers replaced bilateral nephrectomy as a treatment of hypertension.

Indications of Dialysis

1- Fluid overload.

2- Sever acidosis.

3- Hyperkalemia.

4- Metabolic encephalopathy.

5- Pericarditis.

6- Refractory GIT symptoms.

7- Drug toxicity.

8- Coagulopathies.

Preoperative Evaluation General Roles:# Optimization of the patient depends on Hemo-

dialysis.# Regardless of the surgical procedure, or the type of

Anesthesia employed, complete evaluation is required to make certain that Pt. Is in optimal condition.

# Reversal manifestation of uremia should be controlled by dialysis a day before. Drugs should be continued.

# Physical, and Lap evaluation should focus on cardio-respiratory functions.

Physical and Lap. Evaluation

1- WT. Of the Pt. before and after dialysis.

2- Chest X ray film.

3- ABG for hypoxia, and metabolic evaluation.

4- ECG to evaluate electrolytes, conductive block, LVH, and ischeamia.

5- Echocardiography to evaluate EF, Quantitate LVH, wall motion abnormalities, pericardial fluid.

6- preparation for blood transfusion, if HB < 6-7/dl.

7- Bleeding, and coagulation profiles are essential specially for regional anesthesia .

8- Serum electrolytes, and BUN (more important thane s.creat.), to insure adequate dialysis.

9- Glucose tolerance to to evaluate the need of intraoperative insulin.

10- Drug therapy should be carefully reviewed for drugs with significant renal elimination.

Pharmacological Alteration In CRF

The pharmacokinetic, and dynamic are altered during renal failure for many reasons.

1- Decreased plasma protein specially albumin, can increase the free part of active drug.

2- Acidosis alter the Pka of the drugs, and its degree of ionization.

3- increased vol. Over load alter distribution, and redistribution of the drugs.

4- Azotemia, electrolytes imbalance,and concomitant drug therapy may potentiat the pharmacodynamics of drugs.

5- Renal elimination of the drugs, its metabolites, which may be active prolong its half life.

Premedications# The dose of Opioids (morphine, & Meperidine), and

Bezodiazpines have to be reduced.

# Promethazine 12.5- 25 mg I.M has double benefits as antiemietic and sedative.

# H2 receptor blockers have to be considered in Pt. With nausea, and vomiting.

# Metclopramide 10 mg I.V for being antiemietic, and fastening gastric empting.

# Ondanesteron 4 mg is a powerful central antiemietic, and decreased opioid’s itching.

Intravenous Anesthetic AgentsInduction Agents:

* Thiopental:

The free fraction of a thiopental induction dose is nearly doubled in patients with renal failure, so normal dose has exaggerated clinical effects .

* Ketamine:

Its hypertensive effect is not desirable.

* Etomidate:

Has less cardiovascular depressive effects, this make its large free part with no clinical effect.

* Propofol:

Undergoes extensive, rapid hepatic biotransformation to inactive metabolites that are renally excreted. Its pharmacokinetics appear to be unchanged in patients with renal failure.

* Benzodiazepines:

It would seem that a single dose of benzodiazepine should be well tolerated but that the dose should be reduced due to the possibility of increased free fraction, accumulation of active metabolites and increased patient sensitivity.

Opioids:* Fentanyl:

Appears to be an excellent opioid for use in CRF because of its lack of active metabolites, unchanged free fraction, and short redistribution phase.*Alfentanil:

Has reduced protein binding but no change in its elimination half-life or clearance in CRF and is extensively metabolized to inactive compounds.* Sufentanil: Free fraction is unchanged in CRF, but it’s active metabolites ‘excreted by the kidney’ prolongs narcosis in CRF.

Inhalational AnestheticsA part of sevoflurane < enflurane for their toxic

florid ion accumulation making them potentially toxic for long procedures, volatile anesthetics are ideal for renal Pt. Because:

1- Minimal metabolites.

2- Minimal affection of renal blood flow.

3- Controlling blood pressure.

But MAC is decreased, enhancing induction, delaying recovery due in part to marked anemia (HB< 6 g/dL.), and increased blood gas partion coefficient.

Nitrous oxide:

If used not more than 50%………why?

- Circulation is hyperdynamic.

- Fio2 must increased to allow more o2 to dissolve in plasma, in the presence of marked anemia.

* Succinylcholine:-K+ level should be < 5 MEq/L. -Its action may be prolonged due to decrease level of psudocholinestrares after dialysis.

-* The older nondepolarizing NMBAs: (i.e., d-tubocurarine, metocurine, pancuronium, and gallamine) all have prolonged elimination half-lives in renal failure.

Neuromuscular Blocking Agents

* Long-acting NMBAs (as pipecuronium):

This group has an unpredictable response, with a wide variability in duration of action.

*The intermediate-acting NMBAs.

- Atracurium, and Cis-atracurium:

Undergo enzymatic ester hydrolysis and spontaneous nonenzymatic (Hoffman) degradation with minimal renal excretion of the parent compound. Their elimination half-life, clearance, and duration of action are not affected by renal failure nor have they been reported to cause prolonged clinical effect in CRF.

-Vecuronium:

The duration of action is prolonged as a result of reduced plasma clearance and increased elimination half-life. As the drug has active metabolite, 3-desmethylvecuronium, it is not recommended for I.v infusion.

-Rocuronium:

- There is increased rocuronium’s volume of distribution and elimination half-life, but no effect on its clearance in CRF.

- Wide variation in the duration of neuromuscular block has been reported.

Reversal of Muscle Relaxant* Anticholinesterases:

Neostigmine, Pyridostigmine, and Edrophonium are significantly affected by renal failure. All three have a prolonged duration of action in CRF due to their heavy reliance on renal excretion.

* Anticholinergic:Atropine and Glycopyrrolate, are similarly

excreted by the kidney. Scopolamine is the least renal dependant but azotemia enhances its effects.

Therefore, no dosage alteration of the anticholinesterases is required .

Other Drugs

* Phenothiazine:

Dropredol depends on renal excretion, the dose should be < 2.5 mg. The drug is metabolized in the liver, but its effect is enhanced by Azotemia.

* Diuretics, & digitalis.

* Antihypertensive: Ca++ ,& B blockers, clonidine, and AC inhibitors.

* Antiarrhythmic: Procainamide, & Bretylium.

*Antibiotics: Penicillin, Cephalosporins, Vancomycine, and Aminoglycosid.

* Anticonvulsant: Carbamazepine, Primidone.

* Antipsychatric: Lithum.

Together with Terbutaline are accumulated in CRF.

Monitoring

- Non invasive Bp is applied to the limb with no shunt.

- In major surgery direct arterial pressure, CVP,& PAP is useful specially if the Pt is diabetic.

Induction of Anesthesia-The dose of induction agents should be reduced.

-Full dose of muscle relaxant.

-Rapid sequence intubation, with cricoid pressure.

- Suppression of stress response to intubation by I.V Lidocaine, and/ or esmolol.

Maintenance of Anesthesia

-The aim is to control Bp. With minimal effect on the COP as it compensates for anemia.

A balanced narcotic biased anesthesia, with adequate muscle relaxation, and Inhalational, or I.V anesthetics is a satisfactory technique.

-N2O is not used where LVH , and / or HB < 7g/dl. Exist.

Mechanical Ventilation

Controlled ventilation with normocapnia is much better than development of acidosis during spontaneous breathing, or respiratory alkalosis if hypocapnia occurs with consequent decrease in CBF, and hypocalcaemia.

 

Fluid Therapy

- Infusion of 1L. Of RL adds 4MEq K+ , that is why it is not suitable.

- Glucose biased solution is not suitable for diabetic Pt., otherwise it is good to replace insensible loss.

- Nacl is adequate fluid to be used.

- Blood transfusion has no effect, but may be beneficial in renal transplantation.

- Albumin can be used via central line to raise CVP.

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