CASE REPORT

Topic : Altered Mental State

Presented by :
Larasati Rahmania
Melany

Supervisor :
dr. Ali Haedar, Sp. EM
Emergency Department of Medical Faculty Brawijaya University
2016
BACKGROUND 2

AMS may be found in 4%

10% of Emergency
Deparment patients,
From the 1.934 AMS patients
collected:
1. Their age ranged from 14
to 97 years (average age
51.9515.71 years). First
peak at 33 years and
second peak at 72 years
2. Total mortality rate was
8.1% .The death rate was
higher in elderly patients
(60) than in younger
(Studied from World J. Emerg. Med., patients (10.8% vs 6.9%)
Medical College Hospital, Chinese
Academy, China, 2012)
 CONTD

Altered mental status (AMS) is a very common

emergency case, but the exact etiology of many AMS
patients is unknown. Patients often manifest vague
symptoms, thus, AMS diagnosis and treatment are highly
challenging for emergency physicians. The aim of this
discussion is to provide a framework for the assessment of
AMS patients. This discussion is very important because it
can give more information about the etiology, clinical signs
& symptoms of mental status changes and therefore
improve diagnostic skills and management.
PATIENT IDENTITY

Name : Mrs. S
Age : 65 years old
Address : Ds. Argosari RT 5/1 Jabung Malang
Occupation : Housewife
Religion : Islam
Reg. Number : 113021xx

Patient came to ER on July 28th, 2016 at 15.30 WIB

PRIMARY SURVEY

A : Patent, additional breathing sound (-)

B : Symmetrical chest expansion, RR 22 tpm, regular, retraction (-),
SaO2 92%

C : BP 160/130 mmHg, HR 93 bpm, regular strong, warm acral, CRT <

2
D : GCS 345, Pupil round isokor 3mm/3mm
E : Axilary temperature 36C, RBS 141 mg/dl

Triage Priority: P1
INITIAL TREATMENT

A :-

B : O2 10 lpm via NRBM

C : Head of bed elevation 30, IVFD NaCl 0.9% 20 tpm
D :-
E :-
ANAMNESIS
HETEROANAMNESIS FROM HER DAUGHTER

Chief complaint: Decrease of consciousness

History of present illness: Patient suffered decrease of consciousness
since 2 hours before admission. At first, she complained severe headache,
accompanied by nausea and vomiting continuously since 7 hours before
admission. History of fever, seizures, and shortness of breath were denied.
Past medical history: History of hypertension known since 8 years ago.
She didnt routinely control and consume medication. History of diabetes and
trauma were denied. History of previous decrease of consciousness was denied.
Family history: History of family with diabetes and hypertension were
unknown.
Social history: The patient was a housewife, married, and has two
children. She didnt smoke.
 PHYSICAL EXAMINATION
General appearance: severely ill BW 60 kg Height 160 cm
GCS 345 BMI 23,4 kg/m2
BP = 160/130 PR = 93 bpm regular, RR = 22 tpm Tax : 360C
mmHg strong
Head Conjunctiva Anemic (-) Pupil isochoric 3/3mm Dry tounge
Sclera Icteric (-)
Neck JVP flat Lnn. Enlargement (-)
Thorax
Cor S1 S2 single regular, murmur (-), gallop (-)
Pulmo Symmetri Stem fremitus Ves + Rales - - Wh - -
c D=S +
+ - - - -
+
+ - - - -
+
Abdomen Flat, soefl, Bowel Sound (+) N, tenderness (-)
Extremities Warm Edema - -
acral
CRT < 2 - -
NEUROLOGICAL EXAMINATION

GCS 345
Meningeal Sign Neck Stiffness (+) Kernig Sign ( - | Brudzinski I, III, IV (-)
-) II (+)
Cranial Nerves Point Result
N. I Not evaluate
N. II Visus Difficult to evaluate
Confrontation Difficult to evaluate
Ischihara Difficult to evaluate
Funduscope Not evaluate
N. III, IV, VI Ptosis (-)
GBM Difficult to evaluate
Accomodation Difficult to evaluate
Pupil PBI 3mm|3mm
Light Reflex +|+
Cranial Nerves Point Result

N. V Sensoric Difficult to evaluate

Motoric Difficult to evaluate

Reflex Difficult to evaluate

N. VII Sensoric Difficult to evaluate

Motoric Difficult to evaluate

N. VIII Auditoric Difficult to evaluate

Vestibulary Difficult to evaluate

N. IX, X Vernet Rideau -

Vomiting Reflex -

Dysfonia -

N. XI Sternocleidomastoideus Difficult to evaluate

Trapezius Difficult to evaluate

N. XII Sensoric Difficult to evaluate

Motoric Difficult to evaluate

Dysartria Difficult to evaluate

 Bicep +2 | +2 Motoric
Tonus
Physiolog Tricep Power
+2 | +2

ic Reflex Knee N|N

+2 | +2 Lateralization
N|N (-)
Archilles +2 | +2

Tromner -|-
Sensoric
Hoffman -|- Difficult to evaluate
Pathologi
c Reflex Babinski +|-
Autonom
Chaddock -|-
Catheter
Oppenheim - | - (+)

Gordon -|-
Conclusion :
Schuffner -|- There is neurological disorder which is
showed by positive finding of
Gonda -|- pathologic reflex on babinsky of the
right extremity and also positive
finding in meningeal sign
LABORATORY EXAMINATION

Lab Value Normal

Leucocyte 13,79 4,7-11,3 103/l
Haemoglobin 16,5 11,4 15,1 gr/dl
Hematocrit 47,9 38 - 42 %
Platelet 317 142-424 103/l
MCV/MCH 90,5/31,2 80-93/27-31
Diff Count 0/0,2/92,4/3,6/3, 0-4/0-1/5-67/25-33/2-5
8
RBS 141 < 200 mg/dl
SGOT/SGPT 83/21 0-32/0-33 U/l
Ureum/Creatinine 20,2/0,54 16,6-48,5/< 1,2 mg/dl
 BGA

pH 7,36 7,35-7,45
pCO2 32,8 35-45 mmHg
pO2 83,1 80-100 mmHg
Bicarbonat 18,8 21-28 mmol/L
BE -6,8 (-3)-(+3) Mmol/L
Sat O2 96 % >95%

The patients blood gas analysis show an acid-base disturbance process which is
metabolic acidosis that can be caused of hypoxia process in the patient
ECG

Sinus rhythm, heart rate 93 bpm

Frontal Axis : Left axis
deviation
Horizontal Axis : counter clock
wise
PR interval : 0,12
QRS complex : 0,12
QT interval : 0,28
Conclusion : Sinus rhythm
with heart rate 93 bpm, LVH
CHEST XRAY 28/07/16

AP position, symmetric
Trachea in the middle, bone normal
Right and left phrenico-costalis angle are sharp
Right and left hemi diaphragm are dome shaped
Lung: Normal
Cor: enlarged size, CTR 65%
Conclusion: Cardiomegaly
 HEAD CT SCAN 28/07/16
Conclusion :
- ICH in left frontal lobe, volume 91,9 cc
- SDH in left frontotemporal lobe, density 8,7
mm
- IVH in right and left lateral ventricle with right
lateral ventriculomegaly
- SAH in frontal right lobe, left temporal,
anterior falk cerebral, and left prepontin
cysterna
- Cerebral edema with subfalcine herniation to
the right 9,3 mm and transtentorial
herniation downward in mesencephalon level
DISCUSSION
PRIMARY SURVEY

A: no abnormality
B: slightly tachypneu 22 tpm, rapid and shallow breathing pattern
C: hypertension160/130 mmHg, slightly tachycardi 93 bpm
D: decrease of consciousness with GCS 345
E: no abnormality
Triage priority: Red Zone (P1)
INITIAL TREATMENT

A :-

B : O2 10 lpm via NRBM

C : Head of bed elevation 32- 45 , IVFD NaCl 0.9% 20 tpm
D :-
E :-
ANAMNESIS
HETEROANAMNESIS FROM HER DAUGHTER

Chief complaint: Decrease of consciousness

History of present illness: Patient suffered decrease of consciousness
since 2 hours before admission. Previously, she complained severe headache,
accompanied by nausea and vomiting continuously since 7 hours before
admission. History of fever, seizures, and shortness of breath were denied.
Physical examination: GCS 345

Discussion:
Based on the chief complaint in the patient, the patient had decreased of
consciousness with opened eye respond with word, look confused, and motor
respond to localize pain (GCS 345) which is categorized as altered mental
state.
DEFINITION

An alteration in mental status refers to general changes in brain

function, such asconfusion, amnesia (memory loss), loss of alertness,
loss of orientation (not recognize of self, time, or place), defects in
judgment or thought, unusual or strange behavior, poor regulation of
emotions, and disruptions in perception, psychomotor skills, and
behavior (Harrison's Principles of Internal Medicine, 19th, 2015)
ANAMNESIS
HETEROANAMNESIS FROM HER DAUGHTER

Chief complaint: Decrease of consciousness

History of present illness: Patient suffered decrease of consciousness since 2 hours
before admission. Previously, she complained severe headache, accompanied by nausea
and vomiting continuously since 7 hours before admission.
Past medical history: History of uncontrolled hypertension known since 8 years ago.
Neurological examination: GCS 345, meningeal sign neck stiffness (+), Brudzinski
II (+),
Pathological reflex babinsky + l
Discussion:
Based on anamnesis, patient complained severe headache and vomiting before decrease of
consciousness, and from the neurological examination there is sign of brain damage which
is found as positive meningeal and Babinski sign. This indicated that altered mental state
can be caused by structural damage of the brain. Also in the patient, history of uncontrolled
hypertension can provide the risk factor of brain vessel rupture which can cause structural
damage of the brain.
 24

DETERMINE THE CAUSE

Non structural causes Structural causes

Empty pill container Complained of headache to family/friends
prior AMS
Medical diseases, e.g. epilepsy, liver disease, History of brain tumor
diabetes, etc.
Possible exposure of CO Trauma
Absence of focal neurological sign Presence of focal neurological sign
Sign of metabolic acidosis Head trauma
Anticholinergic sign

(Peter Manning & Goh Ee ling,

2015)
 APPROACH TO CLINICAL DIAGNOSIS OF ALTERED MENTAL STATE

Altered Mental state

Airway Check Sp O2
Breathing Give 100 % O2
Circulation Check Pulse

Vital Sign/temperature
ECG monitor
Bedside glucose

Targeted history and physical examination

- Head injury
Structural cause - Neck stiffness Toxic/metabolic
- Respiration rate and pupil size cause
- Chronic organ failure sign
25
 Structural cause Toxic/metabolic cause

Head trauma Afebrile

Intracranial Poisons
Febrile:
hemorhage Non head trauma : - Drug overdose; Opioid,
- Cerebral abcess
- Intracranial hemorrhage BZD,barbiturate,TCA,ketamine
- Meningitis
- Subarachnoid hemorrhage - Alcohol intoxication
- Encephalitis
- Brainstem stroke - Wernickes encephalopathy
- Cerebral malaria
- Cerebellar stroke - Carbon monoxide
- Bacteraemia
- Cerebral tumor Metabolic
- Septicaemia
- hypoglicemia, cerebral
- UTI in elderly
hypoperfusion, hypercarbia,
- Heat stroke
diabetic coma, myxoedema
- Thyroid crisis
coma, hypothermia,
dehydration, electrolyte and
acid-base abnormalities

Organ Failure
Uraemia, hepatic, respiratory,
cardiac

Post ictal state

Psychiatric
Psychogenic stupor, dementia
(Peter Manning & Goh Ee ling, 2015) 26
 ANAMNESIS
HETEROANAMNESIS FROM HER DAUGHTER

Chief complaint: Decrease of consciousness

History of present illness: Patient suffered decrease of consciousness since 2
hours before admission. Previously, she complained severe headache,
accompanied by nausea and vomiting continuously since 7 hours before
admission.
Neurological examination: GCS 345, meningeal sign neck stiffness (+),
Brudzinski II (+),
Pathological reflex babinsky + l
Discussion:
Based on the classical symptom which is sudden severe headache thunderclap
headache , nausea & vomiting (sign of increased ICP) and positive findings in
meningeal sign indicate a meningeal irritation, thus can conclude that the patient
had a subarachnoid hemorrhage.
 HEAD CT SCAN 28/07/16
Conclusion :
- ICH in left frontal lobe, volume 91,9 cc
- SDH in left frontotemporal lobe, density 8,7
mm
- IVH in right and left lateral ventricle with right
lateral ventriculomegaly
- SAH in frontal right lobe, left temporal,
anterior falk cerebral, and left prepontin
cysterna
- Cerebral edema with subfalcine herniation to
the right 9,3 mm and transtentorial
herniation downward in mesencephalon level

Discussion:
The CT show that there is a subarachnoid
hemorrhage in the brain that can increase the
intracranial pressure and also disturb the
ECG

Conclusion: Sinus rhythm with

heart rate 93 bpm, LVH

Discussion:
The ecg show a left ventricle
hypertrophy that can be caused
by chronic uncontrolled
hypertension in the patient. The
heart rate is normal, meaning
there isnt any dysfunction as the
complication of the brain damage
yet.
CHEST XRAY 28/07/16

Conclusion: Cardiomegaly

Discussion:
Cardiomegaly of the patient can be caused
by the chronic uncontrolled hypertension,
that can be the risk for cerebral aneurysm
of the brain and cause of subarachnoid
hemorrhage.
PHYSICAL EXAMINATION

BP 160/130 mmHg (3.30 PM) become 165/85 mmHg (6.00 PM) High
systolic blood pressure
HR 93 bpm (3.30 PM) become 80 bpm (6.00 PM) Relative
bradycardia
RR 22 tpm (3.30 PM) become 24 tpm (6.00 PM) Tachypnea

Discussion:
Fulfilling the triad Cushing of the elevated intracranial pressure, high
systolic blood pressure is the mechanism to increase the blood brain
perfusion when the intracranial pressure begin to rise. When the brain blood
flow restored, the heart rate begin to decrease and if the blood flow is also
reduced to brainstem, it can cause an irregular breathing.
CPP (Cerebral Perfusion Pressure) = MAP MIC
MAP = Mean Arterial Blood Pressure
MIC = Mean Intracranial Pressure

Normal value of ICP 7-15 mmHg

Triad Cushing of Elevated Intracranial Pressure (End Stage):

Irregular respirations (caused by impaired brainstem function)
Bradycardi
Systolic hypertension (widening pulse pressure)
(Gaurav, 2015)
Rodon, 2011. Altered Mental Status in Urgent Care Patient. The Journal of Urgent Care
 MANAGEMENT AMS

Initial Treatment Lowering Intracranial Lowering Blood Pressure

1. Maintenance patency Pressure 1. Nimodipine IV 0,2 mg/50 mL
of clear airway 1. Head up 32-45 initial dosage 1mg/hr can be
increased to 2 mg/hr until
2. Supplemental O2 10 2. IV mannitol infuse with 20
lpm NRBM target MAP decrease to 112
% mannitol solution, mmHg with diastolic blood
3. Establish the IV line for dosage 5cc/kgBW pressure no less than 100-
NS 0,9 % 20 tpm 110 mmHg in one hour
WORKING DIAGNOSIS

From primary survey and secondary survey which

include anamnesis, physical examination and also further
diagnostic evaluation, we diagnosed tha patient:
AMS dt SAH dd SDH, ICH, IVH

Dispose to Neurosurgery Departement

LESSON LEARNED

AMS divided as structural and toxic/metabolic causes, but the first important thing is
the primary survey of the patient (A,B, C)
The antihypertensive agent for SAH must be selectively chosen because each
antihypertensive agent has their contraindication for some situation, e: Nitrat can
cause vasodilatation that increase ICP in patient with SAH, diltiazem in
contraindicated with heart failure condition
For AMS dt SAH must be aware for increasing ICP so the treatment must be lowering
ICP, lowering blood pressure (MAP) to increase the cerebral perfusion (CPP)
There are some ways to lower intracranial pressure; mechanical way (elevated head
up 32-45 degree), pharmacology (hyperosmolar, hypertonic or hypertonic lactat
solution) and also surgical method if required.
THANK YOU