Interesting case

conference
May 26th, 2016

Wachira Wongtanasarasin, M.D.

Department of Emergency Medicine, CMU

Case presentation
A Thai male 33-year-old

Acute visual loss 12 hours prior to

arrival

Initial assessment and stabilization

A: Can talk, no stridor
B: Clear, equal breath sound both lungs
RR 26 /min, SpO2 98% (RA)
C: BP 158/110 mmHg, HR 116 bpm
CRT 1 sec, warm skin, full peripheral pulse
D: E4V5M6, agitation, pupil 4 mm BRTL
E: BT 36.0 c

Initial assessment and stabilization

No immediate life-threatening condition

IV access
Monitoring BP, HR, Oxygen saturation
Dtx = 127 mg%

History taking ?

Acute visual loss

How we taking the history ?
Categorize the symptom

Visual loss
Change in appearance of eye
Eye pain/discomfort
Trauma: Mechanism

Onset: sudden or gradual

Duration
Monocular/Binocular

Circumstances surrounding
the onset
Painful/painless
Characteristic of pain: aching,
burning, throbbing
Pruritus
FB sensation
Flashing light

Past history
Previous surgery
Contact lens
Chronic use of certain
ophthalmic medications
History of diabetes, HT
Previous similar symptoms
and associated diagnosis

History taking
12 hr PTA, after drinking alcohol (bootleg whisky), he
complained to his mother that his vision decreased
bilaterally. His mother told him to sleep for a while.
10 min PTA, He developed severe back pain. His
consciousness was good. He denied history of back
trauma. His vision progressively decreased at that time
His mother stated that he was agitation and sweat out
over extremities. He also put his hands on the chest.
At the emergency room, he was restless and excessive
sweating

Past medical history

No known underlying disease

No current medication
Denied history of eye trauma/FB
Denied history of using contact lens
Chronic alcohol drinking (5+ years)
Denied history of herbs or over-the-counter
drug used
Denied history of refractive error

Physical examination
V/S: BP 158/105 mmHg
HR 115 bpm
RR 30 /min
SpO2 99 %
BT 36 c
HEENT: No pale conjunctivae, anicteric sclerae,
cervical LN cant be palpated, no jugular venous
distension, no carotid bruit
Lungs: clear and equal breath sound
Heart: Regular tachycardia, normal S1S2, no murmur
Abdomen: normoactive bowel sound, soft, no
tenderness

Physical examination
During a neurological examination
He was drowsiness and
unresponsed

Re-assessment
A: Air hunger
B: RR 36 /min, SpO2 90%
lungs: clear and equal BS
C: BP 170/110 mmHg, HR 120 bpm, CRT 1 sec
warm extremities
D: E1V1M4 pupil 4 mm SRTLBE

CXR portable

Whats next ?

Neurological assessment
in coma patient
CPOMR
Consciousness: normal, confused, drowsy, stuporous, semicoma, coma
Pupils
Ocular movement and eyelids
Primary position
Spontaneous/reflex eye movement

Motor system
Limb position, spontaneous movement
Seizure activity
Muscle tone, motor response, posture

Respiration

In this patient
C: Drowsiness, E4VTM5
P: Pupil 4 mm SRTLBE
O: Eye opening, Spontaneous eye movement,
midline primary position, Intact Dolls eye sign
M: Spontaneous equal movement, Motor
power at least Gr. III all
R: Normal pattern but hyperventilation

What is your idea ?

Acute altered mental status

Intracranial

Stroke/TIA
Seizure/Post-ictal phase
SAH
Intracranial hemorrhage
CNS mass lesion
Subdural hematoma
Meningitis/Encephalitis

Extracranial

Encephalopathy: septic, uremic,

hepatic, hypertensive
Metabolic/toxin

Hypo/hyperglycemia
Toxic alcohols
Electrolyte abnormalities
Hepatic/Uremic encephalopathy
Thyroid disorders
Hypoxia/Acidosis

Environment: hypo/hyperthermia

CT brain (non-contrast)

CT brain (non-contrast)
FINDINGS: The study shows
- Normal attenuation of brain parenchyma without focal lesion.
- Normal appearance of ventricular system, cisterns and cortical
sulci.
- No shift of the midline structures.
- Mucosal thickening in right maxillary sinus. A dome shape soft
tissue lesion in right sphenoid sinus is likely to be mucosal retention
cyst. The remaining PNSs and bilateral mastoid air cells appear
normal.
- The bony calvaria are intact.
IMPRESSION:
- No evidence of intracranial hemorrhage or large territorial
infarction.

Laboratory investigation

Laboratory investigation

Laboratory investigation

Laboratory investigation
UA

12-lead EKG

What info. you get

from the labs ?

What info. you get

from the labs ?
Metabolic acidosis
- Anion gap = 142-104-5 = 33
High-gap metabolic acidosis
3312 21

- Delta ratio =
=
=
= 1.1
3
245
19
Pure high-gap metabolic acidosis
- Calculated osmolarity = 2[Na] +
= 2(142) +

196
18

6
0.8

18

0.8

= 302.3

- Osmol gap = Measured osmolality calculated osmolarity

= 346-302.3 = 43.7 High osmol gap
Lactic acidosis
AKI
Hyperphosphatemia

Put it all together

Most likely diagnosis ?

Serum methanol, Ethanol

Diagnosis
Severe high gap metabolic acidosis from
methanol intoxication
DDx. Lactic acidosis, AKA
AKI
Acute visual loss suspected from methanol
intoxication

Management
Bicarbonate administration (at ED total 300 ml
of 7.5% NaHCO3)
IV fluid
5% D/NSS/2 iv 60 ml/hr
NSS 80 ml/hr

Admit to ICU for CRRT

Case progression
Extubation 2 days after admission
Consult
ophthalmologist
at ward for exam

Case progression

Case progression

Discharge from hospital 7 days after admission

Methanol
Intoxication

Outline
Mechanism and clinical features
Options for treatment
High-gap metabolic acidosis

Methanol

Antifreeze (window washer fluid)

Anti icing agent
Octane booster
Ethanol denaturant
Extraction agent
Solvent
Fuel source
Industrial solvent
Vanish and paint removers
Manufacture of acetic acid, formaldehyde, inorganic
acids

Mechanism and pathophysiology

Rapidly absorbed
Peak level achieved within
30-60 mins
Without treatment, minimal
lethal dose approx. 1 mg/kg
The dose required to cause
permanent visual
impairment in an adult is
estimated to be about a
mouthful (24 gm or 30 mL)

Clinical features
CNS depression: headache, vertigo, dizziness,
seizures, coma
Metabolic acidosis: tachypnea, shortness of
breath to compensate
Visual impairment: photophobia, blurred or
snow field vision, papilledema
Optic neuropathy, Putamen necrosis
Delayed parkinsonism, polyneuropathy
CVS: tachycardia, hypotension
GI: Abd pain, N/V, mild transaminitis
Etc: Rhabdomyolysis, renal failure

Clinical features

Treatment
Three treatment goals
1. Correction of metabolic acidosis with
bicarbonate
2. ADH enzyme blockade, inhibits the
metabolism to toxic metabolites
3. Removal of the parent alcohol and its
metabolite

Metabolic blockade
Fomepizole
Initial dose: 15 mg/kg IV
over 30 min
Followed by 10 mg/kg IV
over 30 min q 12 hr
Until methanol level <6
mmol/L
More frequent dose if
hemodialysis (q 4 hr)
Less S/E: mild nausea,
headache, dizziness

Ethanol
Can be administered IV/PO
Maintain target ethanol
level of 100-150 mg/dL
Monitor serum ethanol q
1-2 hr
Dosing varies depending
on patients baseline
ethanol use

Hemodialysis

Adjunctive therapy
Vitamin B (including folate)

High anion gap metabolic acidosis

Anion gap = [Na+] [Cl-] [HCO3-]

High anion gap metabolic acidosis

High anion gap metabolic acidosis

High anion gap metabolic acidosis

High anion gap metabolic acidosis

Take Home Message

Methanol intoxication is the life-threatening
condition associated with higher morbidity
and mortality
Acute altered mental status with metabolic
acidosis need to investigate including toxic
alcohol ingestion
Prognosis of methanol ingestion correlates
with the degree of acidosis, time to
presentation, initiation of treatment

References

2557 ; 29(1-2) : 81-88

Coma ..
- .. 2550 15 1