Book 6, Case 8-AV fistula, uremia Flashcards
Systemic effects of chronic renal failure, and GO!
Electrolyte: Chronic renal failure is commonly associated with metabolic derangements
that include hyperkalemia, hyponatremia, hypocalcemia, hypermagnesemia,
hypoalbuminemia, uric acid accumulation, and metabolic acidosis.
CV: Long standing metabolic
abnormalities can result in multiple systemic effects such as peripheral and autonomic
neuropathy, cardiac arrhythmias, conduction blocks, accelerated atherosclerosis (hypertension
also contributes), and uremic pericarditis.
Renal retention of sodium and water combined with activation of the renin-angiotensin-aldosterone system often leads to hypertension, with
subsequent left ventricular hypertrophy, congestive heart failure (secondary to HTN, fluid
overload, anemia, and metabolic acidosis), coronary artery disease (disordered fat and
glucose metabolism contributes)
Neuro: metabolic abnormalities can result in seizures, uremic encephalopathy,
GI: anorexia, delayed gastric emptying,
Endo: insulin
resistance
Pulmonary: Increased alveolar capillary
permeability and volume overload may lead to pulmonary edema and restrictive pulmonary
dysfunction.
Insufficient renal production of
erythropoietin, bone marrow suppression, gastrointestinal bleeding, hemodilution, and
chronic infection leads to anemia when the GFR decreased to< 30 mL/min. Finally,
impaired platelet function may lead to bleeding, despite a normal platelet count, PT, and
PTT.
Work up you want on a renal pt?
CBC BMP CXR to r/o pulmonary edema TTE if available-wouldn't delay case for it EKG Coags if we're doing a block
Is ordering a serum sodium level necessary?
Obtaining a sodium level is necessary due to the association of hyponatremia
with CRF. While CRF results in sodium retention, the retention of a disproportionately
larger volume of water can lead to hypervolemic, hypotonic, hyponatremia. It is important to
identify significant hyponatremia due to the associated risk of cardiopulmonary arrest,
cerebral edema, seizures, coma, brain stem herniation, and death. If his sodium level were
low, I would review the patient’s previous sodium levels and examine him for any signs or
symptoms of significant hyponatremia, such as nausea and vomiting, fatigue, lethargy,
headache, confusion, anorexia, uncharacteristic irritability, restlessness, muscle weakness, or
other changes in mental status
If the serum sodium were 130 mEq/L, would you cancel the case? What if it were 120
mEq/L?
Everything depends on the urgency of the procedure. I would like to see the pts baseline sodium and rule out any changes due to hyponatremia If his serum sodium level were 120 mEq/L, I would delay the case for treatment, recognizing
that serum sodium levels below 123 mEq/L (some sources say 120 mEq/L) may result in
serious manifestations of hyponatremia (i.e. cerebral edema, cardiopulmonary arrest,
seizures, coma, and brain stem herniation) despite the compensatory mechanisms associated
with chronic hyponatremia.
Obtaining intravenous access is difficult and the patient is becoming anxious. Would
you administer an intramuscular dose of benzodiazepine?
While I would consider administering a benzodiazepine to help reduce his
anxiety and facilitate the placement of an intravenous catheter, I would avoid an
intramuscular injection, if possible, due to the reduced muscle mass and uremic platelet
dysfunction associated with CRF.Instead, I would attempt to reassure the patient and
administer a reduced dose of benzodiazepine via the oral route
Midazolam: increased free fraction of this extensively protein-bound drug are likely result in an exaggerated clinical affect
Pt won’t let you stick him again-you gonna use his dialysis catheter?
If the patient refused any further attempts to obtain intravenous access, I
would consider utilizing his temporary dialysis catheter, recognizing that this would increase
the risk of infection and/or clotting of this vital access site. To prevent these complications, I
would be very careful to access this site aseptically; leave the line heparinized and aspirate
prior to connecting to an intravenous line; and re-heparinize the line and aseptically seal it at
the time of disconnection.
Interscalene: What are indications, and What does it spare?
operations involving the shoulder, upper and lower arm
can spare C8 and T1
Complications specific: PTX, spinal block
Hoarseness
Phrenic nerve paralysis
Horner’s syndrome (mitosis, ptosis, enopthalmia, nasal stuffiness)
Supraclavicular block: it covers what? cons?
operations involving upper and lower arm, but not the shoulder.
PTX or phrenic nerve block
Infraclavicular block: what for?
upper arm and lower arm but not shoulder-less risk of phrenic nerve block. Ideal for continuous infusions due to less movement
Cons: multiple injections are required. Musculocutaneous nerve may have already branched off PTX is still a risk
Axillary nerve block:
operations of forearm, wrist, and hand
Also may need a musculocutaneous block
How do you feel about meperidine and sevo for renal pts?
Given the potential CNS toxicity associated with the accumulation of
meperidine’s renally excreted metabolite, normeperidine, I would avoid the administration of
this opioid. When using a narcotic for a patient with CRF, I would prefer to use fentanyl,
who’s pharmacokinetics are less affected by ESRD due to a lack of active metabolites, an
unchanged free fraction, and a short redistribution phase. Likewise, Sevoflurane would not
be my first choice for inhalational anesthetic since the metabolism of this agent may produce
compound A (nephrotoxic in rats) and nephrotoxic levels of inorganic fluoride(> 50
μmol/L).
How does chronic renal failure alter the pharmacological affects of intravenous
anesthetics?
-The physiologic changes associated with CRF have a variable effect on the
pharmacokinetics and pharmacodynamics of intravenous drugs. Drugs that are highly
dependent on renal excretion for clearance of the parent compound or active metabolites may
have an increased duration of action.
-It is important to recognize, however, that an
increased volume of distribution (commonly associated with CRF) and/or altered hepatic
metabolism (some hepatic enzymes are inhibited and others are induced in the setting of
CRF) may affect the duration of action of this latter group as well. Moreover, decreased
protein binding (reduced binding of acidic drugs results in a greater fraction of
pharmacologically active drug), uremic-induced disruption of the blood-brain barrier
(resulting in greater brain penetration), and a synergistic affect with various renally excreted
toxins, often results in increased sensitivity to many intravenous anesthetics.
Renal failure patient hypotensive after induction:
(1) myocardial ischemia, since peripheral vascular disease is
often associated with coronary artery disease; (2) a hyperkalemia-induced dysrhythmia, since
the patient’s potassium is elevated (especially if succinylcholine were used during induction);
(3) cardiac tamponade, since CRF and inadequate dialysis can lead to pericarditis and
pericardia} effusion; ( 4) hypovolemia, secondary to overaggressive dialysis; (5) autonomic
neuropathy, a condition associated with both diabetes mellitus and CRF; (6) the perioperative
continuation of his ACE inhibitor (associated with significant perioperative hypotension); (7)
tension pneumothorax, a risk associated with the placement of an interscalene block; and (8)
allergic reaction (especially if antibiotics were administered).
Upon examination, you note jugular venous distension and muffled heart sounds. What
are you going to do?
The clinical picture of hypotension, jugular venous distention, and muffled
heart sounds are consistent with cardiac tamponade, a condition that may develop when
uremic pericarditis leads to a pericardia! effusion. Therefore, I would alert the surgical team,
deliver 100% oxygen, discontinue any anesthetic drugs that may be contributing to cardiac
depression, administer fluids for volume expansion, consider the administration of
catecholamines, treat any bradycardia (i.e. atropine), request transesophageal
echocardiography to confirm the diagnosis, and correct any significant electrolyte
abnormalities or metabolic acidosis (which can contribute to cardiac depression). While
dialysis could help to resolve a pericardia! effusion, this hemodynamically unstable patient
may require immediate pericardiocentesis or pericardiotomy to relieve cardiac compression.
Renal patients: you give reversal and then
If residual neuromuscular blockade were present despite the administration of
a maximal dose of neostigmine (0.07mg/kg), my differential would include medication error,
excessively profound neuromuscular blockade at the time of anticholinesterase
administration (it is recommended to delay reversal until 25% recovery of neuromuscular
function is indicated by the appearance of the 4th twitch with train-of-four stimulation), and
factors that are known to interfere with neuromuscular blockade reversal. This patient is
taking an aminoglycoside antibiotic, which has been shown to potentiate nondepolarizing
neuromuscular blocking drugs, sometimes making it difficult to achieve adequate reversal of
blockade. Other factors that may interfere with antagonism include hypokalemia,
hypocalcemia, hypermagnesemia, impaired renal excretion of the active neuromuscular
blocking drug, metabolic and respiratory acidosis, calcium channel blockers, and
hypothermia.
