Shana Chiborak RN

Patient Profile

· 46 year old Caucasian male

· Married, father of 2 young children

· No known allergies

· Past medical history of depression (not treated

with medication)

·Had a metal object removed from his eye after

welding in 2003

. was a ½ pack a day smoker (no note of when

he quit.)

· Mechanic

. Lives out of town

The Story

Several hours after ringing in the new year

with his wife, a middle aged man called out for help

from their bathroom. His wife did not hear his calls

as she had gone to bed. The man continued to call

and finally his wife heard him. She found him on

the bathroom floor. He had been vomiting

profusely. He had also been incontinent of stool. He

told her to call for an ambulance. She called 911.

She knew it was going to take a while for the

paramedics to get to her home as they lived out of

town. She did her best to stay calm, and she was

asking him questions but she could see that he

was growing weaker by the minute. He could barely

answer her.

On Arrival to Hospital

Patient was taken to Seven Oaks General

Hospital. On Arrival at 05:49hrs his vital signs were

BP: 70/40

HR: 115

T: 37.5

Spo2: 95% 15 litre RB

Has 2 #14G IV’s of NS wide open

His nail beds are cyanotic

He is incontinent of large quantities of stool

He has intractable vomiting

Alert and oriented x 3

Laboratory Values

Normal SOGH

Na (135-147) 136

K (3.5-5.1) 3.7

Chl (97-106) 95 ˄

CO2(18) 18

Gluc (3.6-6) 11.8 ˄

Urea(2.8-7.1) 6.1

Crt (44-106) 170 ˄

AST (10-32) 48 ˄

ALT(<30) 33 ˄

LDH (63-200) 363 ˄

GGT(5-38) 27

Alk Phos (30-120 106

Chemistry

Normal SOGH

WBC (4.5-11.0) 27.7˄

RBC (4.4-5.9) 5.81

Hgb (140-180) 185˄

Plt (150-450) 250

CBC

What other information do

we want to know?

Has he been feeling unwell?

How much alcohol did he have? It was new years.

What did he eat?

Was he having pain anywhere?

Did he fall in the bathroom?

Urinary output?

Blood sugar?

What is his Arterial blood gas?

Normal Values Admission to SOGH

Ph (7.35-7.45) 7.22

PaCO2 (35-45) 32

PaO2 (80-100) 402

HCO3 (22-26) 14

Arterial Blood Gas Values

Causes of Metabolic Acidosis

Severe diarrhea

Alcohol

Liver failure

Hypoglycemia

Medications

Alcohol level 4.2 (Toxic > 33)

Liver enzymes elevated but not off the chart

Blood sugar 11.8

Toxicology screen showed: Acetaminophen <1

Salicylate <5

TIBC 80.3 (47-72)

Iron 8.9

It was decided that the patient be moved to the Health

Sciences Center medical intensive care unit (MICU) for closer

observation. The patient had received a total of 4 litres of

fluid the patients blood pressure increased briefly to 138/80.

Patient was stable on transport he arrived to the MICU at

0700hrs.

Admission note entered at15:35hrs;

Vital signs on admission;

HR: 126

BP: 105/41 map 61

T: 35.7 Axillae

SpO2: 99% 5l NP

Time to Transfer

And the Decline Continues

In the next 15 minutes his blood pressure drops to

66/38 MAP 44. Phenylephrine is started at 5

mcg/kg/min. Blood pressure came up to 73/43

MAP 45. An Arterial blood gas was sent.

Normal Values Admission to SOGH

On 15L FM

MICU 09:40hrs

On 5L NP

Ph (7.35-7.45) 7.22 7.36

PaCO2 (35-45) 32 32

PaO2 (80-100) 402 136

HCO3 (22-26) 14 18

Blood Work on Admission to MICU

Normal SOGH 0720hrs

WBC (4.5-

11.0)

27.7˄ 28.9

RBC (4.4-

5.9)

5.81 Not

recorded

Hgb (140-

180)

185˄ 166

INR(0.9-1.1) 0.9

PTT(26-36) 26

Normal SOGH 0720hrs MICU

Na(135-147) 136 144

K (3.5-5.1) 3.7 2.9˄

Chl (97-106) 95 110˄

CO2 (22-30) 18˄ 17˄

Gluc (3.6-6) 11.8˄ 8.3

Urea (2.8-7.1) 6.1 6.3

Crt (44-106) 170˄ 177˄

Osmolality 309

Cor. Calcium (2.1-2.6) 2.07˄

Phosphate(0.81-1.45) 0.69˄

Albumin ( 35

Magnesium(0.63-0.94) 0.89

CK (52-175) 202˄

Troponin (<0.01) 0.11˄

Normal SOGH 0720hrs MICU

ALT (<30) 33˄ 25˄

AST (10-32) 48˄ 34˄

ALP (30-120) 106 85

GGT (5-38) 27 21

LDH (63-200) 363˄ 235˄

LA (.55-2.2) 5.6˄

Myog (<50) 377˄

Cortisol (5-23) 1437˄

According to the chart the patient was alert and

oriented and consented to being intubated. He was

sedated with 80mg of propofol and intubated at

1020. (The MICU resident note at 22:00 indicated

that he received 120mg propofol and 50mg of

rocuronium but this was not documented any

where else but here). His settings were AC f-20 tv

700 peep 5 fiO2 1.0.

At 1050 vasopressin was started at 2.4u/h.

A right internal jugular catheter was inserted with

a pulmonary artery catheter. A left vas cath was

also inserted.

The Lines are in by 1200 hrs. During the last 2

hours the patients blood pressure remained labile

requiring a change from phenylephrine to

norepinephrine. This was titrated to keep a MAP

greater than 65. Multiple boluses of lactated

ringers as well as HSA 25% were also given.

The patients MAP’s were documented as low as 45

to as high as 71.

With the PA catheter now inserted it is noted that

the patients core temperature is 34.0 degrees- the

bair hugger was put on at this point.

The first set of Cardiac numbers looked like this;

Normal Values 1200 hrs

PA systolic (20-30 mmHg) 30↑

PA diastolic (5-10 mmHg) 14 ↑

PA Mean (10-15mmHg) 22↑

CVP (2-5mmHg) 13↑

Wedge (5-12 mmHg) 13↑

Cardiac output (4-6 L/min) 16.1↑

Cardiac Index (2.2-4.0 L/min) 8.0 ↑

Stroke volume (60-70ml) 150 ↑

Systemic vascular resistance

(800-1400 dynes/sec/cm-5)

288 ↓↓

Pulmonary Vascular resistance

(100-250 dynes/sec/cm-5)

45↓↓

Blood Pressure (120/80) 128/50

Mean Arterial Pressure

(70-100mmHg)

71

After intubation an x-ray is done for line

placement/ET placement/ an abd x-ray is also done

This is what it showed;

This is

the

stomach

Patient requires sedation and paralyzing to be

synchronus with the ventilator- a Midazolam

infusion at 15mg/hr, with a Fentanyl infusion at

150mcg/hr, and boluses of rocuronium 50mg IV

PRN. In spite of all this he still fights the restraints

and the ventilator and requires multiple boluses of

prn fentanyl and versed. After the lines are

inserted an Orogastric tube and Bardex are

inserted to manage the gastric secretions and

diarrhea. Multiple boluses of HCO3 and Lactated

Ringers along with potassium, magnesium and

phosphate have been given to try and correct the

electrolyte imbalance from these losses. About 2

hours after intubation another ABG is sent.

Stabilization Continues

Normal

Values

Admission

SOGH

Pre-intubation

09:40hrs

Post-

intubation

11:30hrs

Ph (7.35-7.45) 7.22 7.36 7.28

PaCO2 (35-45) 32 32 34

PaO2 (80-100) 402 136 137 (on an

fiO2 of 1.0)

HCO3 (22-26) 14 18 15

As the day progressed the patients

Norepinephrine requirements were increasing. At

2100hrs the Norpeinephrine was at

0.65mcg/kg/min. Vaspopressin was still at

2.4u/hr and there was a continuous bolus running

of Lactated Ringers for MAP goals greater than 65.

At this point another set of cardiac numbers were

obtained. They looked like this;

Normal Values 1200 hrs 2100hrs

PA systolic (20-30 mmHg) 30↑ 32↑

PA diastolic (5-10 mmHg) 14 ↑ 13↑

PA Mean (10-15mmHg) 22↑ 20↑

CVP (2-5mmHg) 13↑ 13↑

Wedge (5-12 mmHg) 13↑ 13↑

Cardiac output (4-6 L/min) 16.1↑ 12.5↑

Cardiac Index (2.2-4.0

L/min)

8.0 ↑ 6.2↑

Stroke volume (60-70ml) 150 ↑ 125↑

Systemic vascular resistance

(800-1400 dynes/sec/cm-5)

288 ↓↓ 320↓↓

Pulmonary Vascular

resistance (100-250

dynes/sec/cm-5)

45↓↓ 58↓↓

Blood Pressure (120/80) 128/50 132/51

Mean Arterial Pressure

(70-100mmHg)

71 68

What goes in should come out??

After being in the MICU for 17 hours the ins and

outs are calculated.

Fluid in 24 313 ml

Bardex 1000 ml

OG 850 ml

Urinary output 681ml.

The decision is made to start CRRT.

Circuit Training

At 02:00hrs on January 3rd the Continuous Renal

Replacement Therapy (CRRT) was started and closely

monitored. The treatment plan was no fluid removal.

It was primarily started to help with electrolyte

balance. The circuit was running smoothly. When the

circuit was discontinued the filter changed color??

The circuit is supposed to look like this while

running;

The filter is supposed to be a nice

dark red

But Instead it Looked Like This!!!

And this was not the Patient

This raised some alarms

and questions but there

was no time to ponder

the patient was

unstable.

Blood work was sent at

0300.

Blood Work at 0300hrs

Normal SOGH 0720hrs 0300

WBC (4.5-

11.0)

27.7˄ 28.9˄ 11.9˄

RBC (4.4-5.9) 5.81 Not recorded

Hgb (140-

180)

185˄ 166 126˄

INR(0.9-1.1) 0.9

PTT(26-36) 26

Normal SOGH 0720hrs MICU 0300

Na(135-147) 136 144 138

K (3.5-5.1) 3.7 2.9˄ 2.8˄

Chl (97-106) 95 110˄ 101

CO2 (22-30) 18˄ 17˄ 22

Gluc (3.6-6) 11.8˄ 8.3 8.2

Urea (2.8-7.1) 6.1 6.3 8.0˄

Crt (44-106) 170˄ 177˄ 188˄

Osmolality 309

Cor. Calcium

(2.1-2.6)

2.07˄ 2.04˄

Phosphate(0.81-

1.45)

0.69˄ 1.61

Albumin ( 35 34

Magnesium(0.63-

0.94)

0.89 1.07

CK (52-175) 202˄

Troponin (<0.01) 0.11˄

Normal SOGH 0720hrs MICU 0300

ALT (<30) 33˄ 25˄

AST (10-32) 48˄ 34˄

ALP (30-120) 106 85

GGT (5-38) 27 21

LDH (63-200) 363˄ 235˄

LA (.55-2.2) 5.6˄ 4.4˄

Myog (<50) 377˄

Cortisol (5-23) 1437˄

Just When you Think you Can Catch up on

Charting……

At 0400hrs January 3rd Vital signs rapidly

deteriorated.

The blood was returned to the patient and the

circuit was stopped.

Heart Rate: Sinus rhythm to sinus tachycardia?,

Blood pressure dropped 90/44 MAP 63, saturation

dropped to 82% (Still on fiO2 of 1.0).

Stat EKG revealed an accelerated junctional rhythm

120-130 BPM

Norepi started to titrate up – 0.7mcg/kg/min- vaso

still at 2.4 u/hr

25% Albumin boluses and Lactated Ringers boluses

for MAP >65.

Unable to maintain saturations greater than 80%- at

0510hrs patient was hand bagged. BP was down to

68/36 MAP 43 sat 82%.

At 0512 Norepi increased to 1.0 mcg/kg/min BP

65/36 MAP 44 Another bolus of fluid was given. Sats

90%.

Over the next hour the Norepi was never lower than

0.8mcg/kg/min. An ABG was sent at 0540hrs;

Normal

Values

Admission

SOGH

Pre-

intubation

09:40hrs

Post-

intubation

11:30hrs

0540am

Jan 3

Ph (7.35-

7.45)

7.22 7.36 7.28 7.27

PaCO2 (35-

45)

32 32 34 37

PaO2 (80-

100)

402 136 137 (on an

fiO2 of 1.0)49 BVM

HCO3 (22-

26)

14 18 15 16

Patients blood pressure stabilized and was

able to go back on ventilator briefly. At change

of shift patients blood pressure dropped yet

again. Multiple efforts at resuscitation were

made ABG at 0815;

Normal Values 0815 Jan3

Ph (7.35-7.45) 7.18

PaCO2 (35-45) 47

PaO2 (80-100) 45

HCO3 (22-26) 17

The decision was made to withdraw

care. The patient died at 0849hrs,

with his wife at his bedside.

The Reveal

Some Very important information was left out to

add to the drama of this patient.

This gentleman actually made himself a cocktail

on New Years Eve that would be his last. He was

planning to end his own life.

He made a milkshake containing 300cc of milk

mixed with…… ¾ of a can of Bergers Paris

Green.

What is this might you ask???

It looks like this;

Not a container I would put my straw into!!

What is This??

39% ARSENIC

28% COPPER plus other substances not significant to this case.

Paris Green was used as an insecticide, fungicide, and

preservatives for hides It has also been used to color

fireworks. It was commonly used to color oil paint in the

1800’s used by impressionist paintings such as Van

Gogh.

A Complex Tale of two potent toxins

Arsenic

*Paris Green is an inorganic trivalent arsenic

compound.

*It is an emerald green crystalline powder.

*Most poisonings are from ingestion.

*Systemic poisoning is primarily due to the Arsenic

content.

*Acute ingestion will produce symptoms in 30-60

minutes. This patient according to chart started to

vomit about 45 min after ingestion.

*Common symptoms with this are a metallic or

garlic taste, vomiting, abdominal pain, dysphagia,

profuse watery diarrhea, intense thirst, electrolyte

disturbances and rapid hypovolemia

*Reported lethal doses of ingested arsenic are from 120-200mg

of arsenic.

* Patient ingested approximately 3000mg of Paris Green

*Normal blood range of Arsenic is 2-23 mcg/L

*There was no Arsenic level on the chart. Urine was sent (which

is the best method for measuring) but the sample came back as

insufficient amount and it was not re- sent.

•Post Mortem levels of arsenic were 3.0x10⁵mcg/L

•A Chelating agent was given to this patient. Dimercaprol was

given IM. Patients dose was 3mg/kg q4hrs. This acts by making

a chemical bond with metal ions making them less chemically

reactive. This complex is then water soluble and easier for the

body to filter out. There have been studies that look at the

benefit of starting the chelating therapies prior to hemodialysis

that show very little difference in kidney excretion vs dialysis. A

chelating agent is best used in functioning kidneys.

Arsenics attack of primary organs a system

review

Gastrointestinal Tract

This patient had a massive amount of diarrhea and vomiting

according to the paramedics records. The abdominal x-ray

that was taken shows the substance ingested. Since arsenic

and copper are both metals they showed up in the stomach

and the first part of the duodenum. On the x-ray

interpretation it stated a “barium like substance seen in the

stomach” .

On Autopsy the green substance was still adhered to the

stomach wall.

Normal Stomach

Paris Green

substance

* There is no clear guideline as to how to

decontaminate the stomach and bowel. Some

research suggests gastric lavage if arsenic is in the

lower GI tract on x-ray, this is suggested only if

within 30min to 1 hour of ingestion. Activated

charcoal may not bind significant amounts of arsenic

but is still used.

Interesting article; Japan 2004. Gastric lavage was

performed on a 54 yo male who ingested 20g of

arsenic trioxide. Health care workers involved in

resuscitation including the paramedics and police all

had symptoms of arsenic inhalation injury. The

contents from the patients emesis was actually

emitting arsine gas which is the result of the arsenic

mixing with the gastric acid. The workers involved

had corneal erosion, laryngitis, contact dermatitis,

eye pain and sore throats- no long term effects were

reported.

Cardiovascular System

Where did all our fluid go?

In 2 days that this patient was here he received a

total- 43 634 ml of fluid. His out put total was

just under 3000 ml plus insensible losses.

Once absorbed arsenic binds to hemoglobin, it is

cleared from the intravascular space within 24

hours and gets concentrated in the liver, kidneys,

spleen, lungs and GI tract. It gets cleared slowly

by the kidneys.

Arsenic inhibits suphydryl containing enzymes by

binding to sulphydryl groups. This causes

extreme endothelial cellular toxicity resulting in

capillary damage, extreme vasodilation and

transudation of plasma.

A Review of our cardiac numbers

Normal Values 1200 hrs 2100hrs

PA systolic (20-30 mmHg) 30↑ 32↑

PA diastolic (5-10 mmHg) 14 ↑ 13↑

PA Mean (10-15mmHg) 22↑ 20↑

CVP (2-5mmHg) 13↑ 13↑

Wedge (5-12 mmHg) 13↑ 13↑

Cardiac output (4-6 L/min) 16.1↑ 12.5↑

Cardiac Index (2.2-4.0 L/min) 8.0 ↑ 6.2↑

Stroke volume (60-70ml) 150 ↑ 125↑

Systemic vascular resistance

(800-1400 dynes/sec/cm-5)288 ↓↓ 320↓↓

Pulmonary Vascular resistance

(100-250 dynes/sec/cm-5)45↓↓ 58↓

Blood Pressure (120/80) 128/50 132/51

Mean Arterial Pressure

(70-100mmHg)71 68

Sympathetic response. The CO is high but we are unable to get the squeeze we need

to maintain a blood pressure. Because of the arsenic it’s like a

tug of war. The sympathetic drive is trying to compensate for

the massive intravascular fluid loss while the arsenic has

made this nearly impossible. The fluid is leaking into the

intravascular space even with large doses of Norepinephrine.

With the sympathetic response there is a massive

catecholamine surge as well. In the autopsy findings this

patients heart indicated subendocardial hemorrhage (SEH)of

the left ventricle. This is a common finding in autopsies of

patients who have been in shock, who have had brain injuries,

and in toxic ingestions. It has been attributed to the massive

catecholamine surge that is released with the sympathetic

response. There is still ongoing research as to the cause of

SEH.

Subendocardial hemorrhage of left ventricle

Drowning in Copper

In combination with the arsenic a large component of the

poison was copper. Together this is copper acetoarsenite.

Copper is a green chemical. It is a strong gastric irritant as

well as a strong oxidizing agent. It will oxidize

oxyhemoglobin from the ferrous to the ferric form. In this

form, hemoglobin loses is oxygen binding capacity resulting

in methemoglobinemia and cyanosis.

To try and defeat this methylene blue was given .

Methylene blue is given as a reducing agent. The

methemoglobin reductase enzyme is reduced by NADPH

causing an affinity to methylene blue. Methylene blue is

reduced through a process to hemoglobin.

The large quantities of fluid required to keep the

blood pressure sustained contributed to the inability

to oxygenate this patient. The arsenic caused the

massive capillary leaks which included the

capillaries that surround the lungs. Gas exchange

was almost obsolete with a PaO2 of 49 on 100%

oxygen. This patient in the end developed Acute

respiratory distress syndrome.

The Green CRRT Filter

The copper that was in very large amounts in the patients

blood circulation is what changed the color of the filter.

Of interesting note a subsequent finding on autopsy

revealed that this patient had suspected viral meningitis.

“There were perivenous inflammatory collections that were

widespread. It was unclear if this inflammation was

secondary to the overdose but there is no biochemical

reason as to why arsenic toxicity would give rise to this

type of inflammation.”

In 2003 Chromated Copper Arsenate; AKA pressure

treated wood was stopped being produced. Why?? Large

quantities of arsenic were being found leached into soil.

This wood was found everywhere. Kids playgrounds,

fences, docks, buildings. Not only the arsenic that was

leaching into the soil was toxic, it was the burning of

this wood that caused real concern!! The burning

actually causes a chemical reaction in the wood. It

releases the truly lethal forms of arsenic. The gases can

cause airway burns, eye irritation and dermatitis. But

more importantly 1 tablespoon of ash in your coffee and

its game over!!!

Why my husband now makes his own coffee

Thank you!

Thank you to the following people who helped

me with my investigation,

Sarah Gilchrist RN BN Clinical educator ICU

Mark Rabnett- Uof M Librarian

Barbara Burr-RN, Medical Examiner Investigator

The Internet☺☺☺☺