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Clin Tox Exam 1 > Salicylate > Flashcards

Salicylate Flashcards

1
Q

Forms of Salicylates

A 
Analgesics
Topical (Oil of wintergreen/ben gay)
Bismuth Subsalicylate (pepto bismol)
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2
Q

Toxic Doses Levels

A

Less than 150: no toxic reaction
150-300: mild to moderate toxic reaction
300-500: Serious toxic reaction
>500 potentially lethal toxic reaction
***>100 mg/kg for 2-3 days: chronic toxicity

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3
Q

Salicylates Absorption/Peak

A

1 hour

Toxic: delayed due to concretion formation

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4
Q

Salicylates Distribution Protein Binding and Vd

A

90% and 0.17 L/kg

Toxic: 75% (more free drug) and 0.35 L/kg

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5
Q

Salicylates Elimination

A

15-20 minutes (dose dependent elimination)

Toxic: up to 30 hours

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6
Q

Normal Salicylate Metabolism

A

10% unchanged in the urine (pH dependent)
90% absorbed protein bound through glycine conjugation, glucuronidation and oxidation (75% of which is glucine conjugation to salicyluric acid)

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7
Q

In Overdose, what happens to Salicylate

A

Only 76% is absorbed and protein bound leaving more to go out into the tissue and be free drug

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8
Q

Acute Toxicity: victim, circumstance, time to diagnosis, mortality, suicide, serum concentration

A 
Young adult
Intentional
Short
Uncommon mortality
Typical
Marked elevation
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9
Q

Chronic toxicity: victim, circumstance, time to diagnosis, mortality, suicide, serum concentration

A 
Elderly
Unintentional
Long
More common mortality
Atypical 
Intermediate elevation
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10
Q

Clinical Presentation Based on Phase of Acute

A

Phase 1: GI upset, tachypnea, hyperventilation, respiratory alkalosis, Na, K and bicarbonate renal secretion, N/V
Phase II: Metabolic acidosis
Phase II: Metabolic and respiratory acidosis, dehydration , severe K and bicarb depletion, coma, seizure, death

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11
Q

Chronic Clinical Presentation

A

More insidiously and may be subtle

Primarily neurologic like confusion, delirium and agitationi

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12
Q

Respiratory Alkalosis Look like

A

pH: 7.51 (high)
pCO2: 27 (low)
HCO3: 21 (low)

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13
Q

Respiratory alkalosis and Metabolic acidosis Looks like:

A

pH: 7.42 (normal)
pCO2: 15 (low)
HCO3: 9.5 (low)

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14
Q

Metabolic acidosis with respiratory acidosis

A

pH: 6.67 (low)
pCO2 (HIGH)
PO2 30 (LOW)
HCO3 9.5 (low)

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15
Q

What happens in respiratory alkalosis?

A

Direct stimulation of the respiratory center of the brain causing hyperventilation which increases depth (hyperpnea) and rate (tachypnea) –> increased CO2 exhalation leads to decreased pCO2 and rise in pH (alkalosis) –> compensatory increase in excretion of bicarbonate eventuating the decrease buffering capacity

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16
Q

***What happens in metabolic acidosis?

A
  1. Uncoupling of oxidative phosphorylation (decreased ATP)
  2. Inhibition of Kerb’s cycle (accumulation)
  3. Fatty acid metabolism (accumulation of ketoacids)
  4. Enhanced glycolysis (accumulation of lactic/pyruvic acid)
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17
Q

Kreb’s Cycle Normal Outcome

A

Acetyl CoA formed by fatty acids or glycolysis to ultimately form 4 NADH molecules

18
Q

Kreb’s Cycle when NADH is too high

A

Acetyl CoA become B-OH butyrate which becomes ketoacids leading to ketoacidosis

19
Q

Glycolysis Normal and with too much NADH

A

N: makes ATP and NADH
A: continues to break down the glucose to pyruvate and lactate –> lactic acidosis
***This process first shows as a increase in glucose but as the glucose is depleted, the level will drop!!

20
Q

Acute VS Chronic effect of Glycolysis

A 
Acute = hyperglycemia
Chronic = hypoglycemia
21
Q

What happens in respiratory acidosis

A

Excess CNS salicylate concentration leads to depressed respiratory center leading to loss of drive to increase respiration to compensate metabolic acidosis causing respiratory acidosis

22
Q

CNS Damage is caused by

A
  1. Neuronal energy depletion from uncoupling of oxidative phosphorylation
  2. Release of apoptosis inducing factors like cytochrome C
  3. Severe cellular metabolic acidosis
  4. Cerebral edema
  5. CNS hypoglycemia
23
Q

Pulmonary SE

A

Due to body try to increase ventilation and get rid of the CO2 (acid) as quickly as possible

24
Q

Hematologic SE

A

Increased bleeding time and PT prolongation

25
Q

Fluid SE

A

Stimulation of the chemoreceptor trigger zone –> N/V

Insensible fluid loss –> increased RR, fever, emesis

26
Q

Electrolyte SE

A

Hypokalemia - Respiratory alkalosis –> increase bicarbonate excretion, increase H+ re-absorption in exchange for K

27
Q

***Serum K+ Depleted leads to

A

Renal re-absorption of K in exchange for H+ –> urine is acidic and we want the urine to be alkalotic

28
Q

Salicylate Toxicity Management Emergency Stabilization

A

Airway: maintain ventilation, reserve intubation for respiratory failure
Breathing: Oxygen supplementation
Circulation: correct dehydration 0.9% saline 10-20 mL/kg/hour over 1-2 hours until good urine flow (3-6 mL/kg/hr)
DONT: 50 g dextrose in each liter of fluid (D5W)

29
Q

Salicylate Toxicity Management: Complete Patient Evaluation

A
  1. History: dose, intent of use, pattern of use, presence of co-ingestants
  2. S/Sx (esp CNS and pulmonary edema)
  3. Labs
30
Q

Salicylate Labs

A
  1. Vitals and metal status
  2. Salicylate Levels Q1-2H until peaked and decline
  3. BMP Q2H until improvement (EKG if hypoK)
  4. ABG or CBF for moderate to severe toxicity
  5. Obtain a CBC, liver enzymes, renal test, INR and PTT
  6. Obtain a CT for altered mental status
  7. Urinalysis to monitor urine pH and specific gravity
31
Q

Done Nomogram

A

Six hours or more after single acute ingestion of NON-enteric coated product
Orally ingested and pH > 7.4

32
Q

Step 3: Treatment to Reduce Absorption

A
  • AC for ALL patients that present within 2 hours of significant ingestion (1g/kg one time then 0.5g/kg Q4H until stable and SAL less than 30)
  • Cathartic (sorbitol): One dose with first dose of A
  • WBI: only in MASSIVE overdose or enteric coated/SR formulation
33
Q

Step 4: Measure to Improve Elimination

A

Decrease pH –> increase non-ionized (free) fraction which increases toxicity
Increase pH –> decreased non-ionized (free) fraction which traps the salicylate

34
Q

Goal pH for Serum Alkalization

A

7.5-7.55

This decreases the free non-ionized form

35
Q

Goal Urine pH for Urine Alkalization

A

7.5-8

Increase the ionized salicylate fraction leads to decrease back diffusion of non-ionized form

36
Q

Bicarbonate Dose

A

1-2 mEq/kg ACTUAL BODY WEIGHT!!

Helps get the salicylate out and into the urine

37
Q

Bicarbonate CI

A

Pulmonary edema

Renal failure

38
Q

**Hemodialysis Indication

A 
Persistent CNS disturbances
Pulmonary or cerebral edema
Congestive heart failure
Renal insufficiency
Progressive deterioration in vital signs
Worsening metabolic acidosis
Severe overdose >100 mg/dL in acute or >60 in chronic
Unresponsive acidosis
39
Q

Supportive Care

A

Seizure: benzo
Coagulopathy with prolong PT or INR: vitamin K
Hyperthermia: cooling fans for severe
Hypokalemia: IV potassium boluses or oral

40
Q

Step 5: Specific Antidote

A

NONE

41
Q

Step 6 Continue Care Monitoring

A

Serum Q2H until decrease from peak for at least 2 measurements or ABG has been stable or improved of at least 2
Blood and urine pH, serum K Q1H while on alkalinization therapy and blood glucose until symptoms resolve
Also do psychiatric and education for the patients

Clin Tox Exam 1 (5 decks)

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