What things increase anion gap?

• (M)ethanol
• (U)remia
• (D)ka
• (P)araldehyde
• (I)soniazid, iron
• (L)actic acid
• (E)thylene glycol
• (S)alicylates

• Cyanide

• CO
• Toluene

Match the order with the possible diagnosis:

• Butter almonds = 

• Carrots =

• Garlic =

• Mothballs =

• Pears =

• Wintergreen =

• Rotten eggs =

Butter almonds =  Cyanide

Carrots = Water hemlock

Garlic = Aresenic, pesticides

Mothballs = Camphor, naphthalene

Pears = Chloral hydrate

Wintergreen = Methylsalicylate

Rotten eggs = H2S

• (D)iarrhea

• (U)urination

• (M)yosis

• (B)ronchoria

• (B)radycardia

• (E)mesis

• (L)acrimation

• (S)alivation

What are causal agents for ACH toxidrome? What is the treatment?

• Agent:  OrganoPO4

• Treatment:  Atropine, Pralidoxime

Red as a beet

Mad as a hatter

Dry as a bone

• Hot
• flushed
• dry
• tachy
• dilated pupils
• seizures
• hallucinations

Basically decreased secretions

NO BOWEL SOUNDS

Agents: 

• Anti-HIS
• Plants (Angel trumpet)
• Cyclics

Treatment

• Physostigmine
• BZDs
• Cooling

• Hot
• Wet
• Tachy

• HTN

• Agitated

• dilated pupils
• Seizures

Anti-Ach = think decrease secretions

Sympatho = Think increase secretions

Anti-Ach = (-) Bowel sounds

Sympatho = (+) bowel sounds

• CNS depression
• Caustics
• Hydrocarbons - worry about chemical pneumonitis
• Seizures
• Foreign body
• Under 6 mo of age

Aspiration

Protracted N/V

Lethary

Cardiomyopathy with chronic use

Life treatening ingestion

within one hour

Aspiration

Constipation

Perforation

Obstruction

Vomiting

Alcohols - (absorbed too fast)

Heavy metals

Iron

Lithium (other small substances)

Potassium

Hydrocarbons

Children:  10/ml/kg/hr (Max = 500 ml/hr)

Adults:  500 ml/hr (Max = 2 L/hr)

Iron ingestion

Lithium ingestion

MDAC failure

Concretions

Body packer/stuffer

sustained release products

Packers = Highly pure substance. Wrapped tightly

Stuffers = People avoiding police. Usually contaminated and not well wrapped

MDAC

urinary alkalinization

HD

50g PO or by GT x 1

Follow with 25 g q6hrs

K+

Gets shifted intracellularly

Low MW

Low Protein binding

Low VD

Water soluble

Air freshners

playdoh

crayons

chalk

calamine lotion

baby lotion/powder

lip balm

glow stick

deodrant

superglue

shoe polish

Silica gel

SX = Immediate burning in mouth and throat

May have GI sx- may pass gas

TX = Home management with dilution

This is very caustic!!!

Serious esophageal and gastric burns

Dysphagia

Drooling

Severe throat/ab/chest pain

Hematemesis and perforation of esophagus/stomach

Hypochlorite + acid = ?

Hypochlorite + NH3 = ?

Chlorine gas

Chloramine gas

Immediate caogulation type necrosis

Forms a eschar to limit further damage

Ca++ and Mg++

Because HF forms a cytotoxic precipitation with those cations

Pain out of proportion on exam

Progressive redness skin blanching

Inhalation causes mucosal irritation

Systemic effects (HypoCa/HypoMg, Hyperk) = arrhythmias

Calcium Gel

10 ES TUMS + 20 ml KY Jelly

Epsom Salt

Calcium Injection

SQ (not in fingertips)

Intra arterial

Ca Gluconate

CaCl2 cases tissue necrosis

Early/aggresive airway management

Anything with Mg or Ca (i.e. milk for dilution)

Continouus EKG monitoring

IV Ca/Mg

Standard therapy for hyperK

Oral mucosal irritation

CNS depression

Mental status changes

Aspiration pneumonitis

If symptomatic (coughing, gagging, vomiting, SOB)

If a high concentration was used (20 - 35%)

1. Local tissue injury (depends on concentration)

2. Gas formation (liberates gas which can cause an Emboli)

N/V - most common, happens immediately with dilute formulation

Ab pain/bloating

Hematemesis (usually w/ higher concentration)

Rapid deterioration in mental status, cyanosis, resp failure, seizures, ischemic EKG changes and acute paraplegia

seizures

renal failure

Boiled lobster appearance

Dispostion based on calculated potential blood alcohol level

Treat at home if < 150 mg/dl  (75 mg/dl if Isopropyl) with a sugar containing beverage

False!!!

They contain Acetonitrile which gets endogenously converted to CN.

As little as 5 mL can be lethal

Treat as if it is an ethanol ingestion.

Usually contain Acetone or Isopropanol

Give a sugary beverage

1 gram of toothpaste = 1 mg of F-

Requires very large ingestion for toxicity = GI effects

Can give 4 to 6 oz of Milk because Ca++ will bind F-

Tremor

Confusion

Seizures ---> Status epilepticus

If >1 mothball then it requires HCF evaluation

Use AC

If it is in the esophagus = Emergent removal by endoscopy to prevent rapid perforation

If in stomach/intestine = Should not be removed unless signs of perforation or obstruction develops

Usually passes uneventuflly within several days

#6

#22

Inhibits conversion of lactate to pyruvate

Inhibits gluconeogenesis

Agonist= GABA A receptor to increase CL- influx

Antag = NMDA to inhibit Ca influx

> 200 mg/dl

 >400 mg/dl

If you suspect a co-ingestion that is amenable to AC.

Have to weigh risk: benefit with respect to aspiration

EtOH increases urinary excretion

Also we have poor dietary intake and decrease GI absorption of Mg

Though to be due to conversion of pyruvate to lactate, diverting pyruvate from gluconeogensis

ETOH increases the redox ratio

HypoNa+

HypoK+

HypoCl-

What are the 3 alcohols that are considered "toxic"?

Methanol

Ethylene Glycol

Isopropanol

CNS depression---> coma

Abdominal Pain "Gastritis"

(acute pancreatitis reported)

Resp. Depression

Weakness

Rhabdo

Depletion of NAD+---> Hypoglycemia

ABCs!!!!!

Decontamination if on skin

NO AC!!!

PPI to help with the gastritis

HD

Acetonemia (Ketoemia)

+ Ketonuria

Increased osmolar gap

+/- hypoglycemia

Oxalic Acid

Hippuric Acid

What is Phase 1 of Ethylene Glycol ingestion? 

What is the time frame of phase 1?

Predominant CNS effects

Altered mental status

Within 4 to 8 hrs

Profound anion gap Metabolic acidosis

(takes about 4-12 hrs)

Acute Renal Failure

May be due to oxalic crystals, but only a small %. 

Other metabolites shown to cause renal tubular damage in vitro.

Osmolar gap

Anion gap metabolic acidosis  (may have a falsely elevated lactic acid because glycolate looks similiar to lactate)

HypoCa+

Renal insufficiency/ARF

Crystalluria

Urine Fluorescence

Monohydrate = Prism/needle like

Dihydrate = Tent or envelope shape

Cardiotoxicity

HypoTN

Bradycardia

Widening of QRS

Death

Propylene glycol is used as a vehicle

Oral

Inhalation

Transdermal

At lower concentrations = First order

At higher concentrations = zero order

False

Considered delayed ~ 24 hrs but can vary up to 72 hrs

Even more delayed if ETOH co ingested

Visual distrubances

Flashes, snowstorms to blindness

Ocular effects may be delayed 12-24 hrs

Dilated pupils

Sluggish light reflex

Hyperemia of optic disks

Retinal edema

EtOH = 4.6

EG = 6.2

MeOH = 3.2

Iso = 6.0

PG = 7.6

Ethanol infusion vs Fomepizole

HD

Cofactors

LD=  8cc/kg   (0.8g/kg)

MD = 1 cc/kg/hr  (130 mg/kg/hr

Competitive inhibitor of Alcohol DH

Has 8000x greater affinity to ADH

What is the dosing regimen for 4MP?

4MP = Fomepizole

LD = 15 mg/kg IV

MD = 10 mg/kg q12 x 4 then 15 mg/kg q12

(In class she said you increase the dose after 48 hrs regardless of how many doses the person received, because you may not be necessarily be giving it exactly every 12 hours)

EG or MeOH level is 0 mg/dl

Metabolic acidosis clears

With EG level > 50 mg/dl

MeOH level >25 mg/dl

(Other source says when either one is above >20 mg/dl)

Or

Wide anion gap metabolic acidosis

Or

Renal injury with EG toxicity

Or

Visual complaints/findings with MeOH toxicity

Give Folinic (or Folic) Acid.

Folinic (or Folic) acid= 50 mg IV q4hrs

or source says 1-2 mg/kg q4 to 6 hrs

Thiamine 50 to 100 mg IV q6hrs

Pyridoxine 50 to 100 mg IV q6hrs

False. That describes EG toxity.

With MeOH toxicity you can expect a WAGMA + Hyperemia of Optic Disc (Visual changes)

Absorption!!

Adults absorb 5 to 10%

Children absorb 40-50 % and retain 20-25%

Bone  --- where the t 1/2 is 20 yrs  (almost impossible to get rid)

Soft tissue ---- where the t 1/2 is 20-30 days  (get rid of with chelating agents)

High affinity for Sulfhydryl groups

Chemically similiar to Ca+ inhibiting Na/K/ATPase

Inhibits ferrochelatase leading to elevated erythrocyte protoporphyrin

Kidneys

Hematopoietic system

Nervous system

Average decline of 2-4 IQ points

Impairment of reading skills

Impairment of academic success (7x increase in failure to graduate from high school)

Greater absenteeism

Lower class standing

ASx = > 10

Mild to moderate = > 50 to 70

Severe = > 70 to 100

Mild = > 40

Moderate = > 80

Severe = > 100 to 150

1. Determine environmental exposure/ hazard reduction

2. Nutritional supplementation

3. Chelation therapy

Check for Iron and Calcim intake

Iron supplementatyion

Take multivitamin with minerals to get trace metals such as copper and zinc

British Anti-Lewisite (BAL)

CaNaEDTA

D-Penicillamine

Dimercaptosuccinic Acid (DMSA)

Inhalation

(remember homie talking about cutting up the rug if you drop some on the floor)

CNS

Pulmonary

Supportive Care

WBI

Chelation

Organic mercury

(Can potentially cause redistribution)

BAL  (CI in organic toxicity tho)

DMSA

BAL

CaNaEDTA

D-Penicillamine

DMSA

Because CaNaEDTA does not cross the BBB

BAL must precede EDTA by 4 hrs

Nephrotoxicity

Delpletion of endogenous metals (Cu, Zn, Fe, Mn)

Transient hypoTN, malaise, HA, anemia

Usually 2 to 6 months

Compliance issues!

In the event of both DMSA and EDTA failure

Used in Lead and Arsenic toxicity

N/V

Rash even SJS

Hemolytic anemia

Thrombocytopenia/leukopenia

N/V/D

Transient elevations in LFTs

rash, pruritus

Hemodynamic Effects

Metabolic effects

CNS effects

Hepatotoxic effects

Capillary leakage

Reduced tissue perfusion

Lactic Acidosis

Cardiac Failure/shock

Direct myocardial damage

N/V/D

Hemorrhagic Gastritis

Intestinal necrosis

Perforation/Peritonitis

Strictures, fibrosis, scarring

Inhibition of Kreb cycle/oxidative processes

Get a buildup of organic acids

Results in hyperglycemia

Onset = 0 to 3 hours

Sx = N/V/D/Ab pain

Lethargy

Restless

Hemetemesis

Onset up to 12 hrs

Quiescent period. But the background things are preparing for the worse

Onset = 12 to 48 hrs

Sx = Shock

Acidosis

Coma

Seizures

Pulmonary edema

Hypogly

Coagulation defects

Onset = 2 to 4 weeks

Sx:  GI Scars and Strictures

What is the % elemental iron content in the following:

Ferrous Gluconate

Ferrous Sulfate

Ferrous Fumarate

Gluconate = 12

Sulfate = 20

Fumurate  = 33

Definitely over 500 mcg/dl

Possible chelation at 350-500 mcg/dl

WBI

Surigcal removal

When serum iron level < 100-150 mcg/dl

 (This target is a little higher to account for the fact Deferoxamine can falsely lower the level. )

Resolution of symptoms

Violent Gastroenteritis with profuse diarrhea and colicky

Ab pain

progression to CV collapse

Dysrhythmias

CNS depression

Onset is 0.5 to 2 hrs

Severe capillary damage with massive 3rd spacing

ARDS

proteinuria

Renal and liver failure

(You basically have no fluids in your vasculature = severe hypotension)

False. Seafood can increase it.

Can see levels up to 200-1700 mcg/l

BAL

D-Penicillamine

Mild = 5 to 7 days

Severe: 10 to 14 days