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 51.95±15.71
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 patients (10.8% vs
(Studied from World J. Emerg. Med., Medical College 6.9%)
Hospital, Chinese Academy, China, 2012)
 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 disscussion is to
provide a framework for the assessment of AMS patients. This disscussion 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 : Moslem
• 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 x/mnt, regular, retraction (-), SaO2 92%
• C : BP 160/130 mmHg, HR 93 x/mnt, regular strong, warm acral, CRT < 2’’
• D : GCS 235, Pupil round isokor 3mm/3mm
• E : Axilary temperature 36°C

Triage Priority: Red Zone (P1)

INITIAL TREATMENT

• A : -
• B : O2 10 lpm via NRBM
•C : Head up 30°, IVFD NaCl 0.9% 20 tpm, Foley catheter and NGT insertion
•D :-
• After conducting a primary survey and initial treatment to the patients, we do secondary
survey (anamnesis, physical examination, and supporting examination)
ANAMNESIS
HETEROANAMNESIS FROM HER DAUGHTER

Chief complaint: Decrease of consciousness

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.
History of hypertension known since 8 years ago. She didn’t routinely control and
consume medication. History of diabetes and trauma were denied. History of previous
decrease of consciousness was denied.
History of family with diabetes and hypertension were unknown.
The patient was a housewife, married, and has two children. She didn’t smoke.
 PHYSICAL EXAMINATION
General appearance: severely ill BW 60 kg Height 160 cm
GCS 235 BMI 23,4 kg/m2
BP = 160/130 mmHg PR = 93 x/m,regular, strong RR = 22 tpm Tax :360C
Head Conjunctiva Anemic (-) Pupil isochoric 3/3mm RC +/+
Sclera Icteric (-)
Neck JVP flat Lmn. Enlargement (-)
Thorax
Cor S1 S2 single regular, murmur (-), gallop (-)
Pulmo Symmetric Stem fremitus D=S Ves + + Rh - - Wh - -
++ - - - -
++ - - - -
Abdomen Flat, soefl, Bowel Sound (+) N,tenderness (-)
Extremities Warm acral Edema - -
CRT < 2’’ - -
NEUROLOGICAL EXAMINATION

GCS 235
Meningeal Sign Neck Stiffness (+) Kernig Sign ( - | - ) Brudzinski I – IV (-)
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 Ø 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
Tricep +2 | +2 Tonus Power
 Physiologic
Reflex Knee +2 | +2 N|N
Lateralization (-)
Archilles +2 | +2 N|N

Tromner -|-  Meningeal Sign

 Sensoris
Hoffman -|- Difficult to evaluate Kaku kuduk +
 Pathologic
Reflex Babinski +|- Brudzinski I -I-
 Autonom
Chaddock -|- Brudzinski II +I+
Catheter (+)
Oppenheim -|-
Conclusion :
Gordon -|- There is neurological
dysfunction which is showed by
Schuffner -|- positive finding of pathologic
Gonda -|- reflex on babinsky of the right
extrimity and also positive
finding in meningeal sign
LABORATORY EXAMINATION

Lab Result Normal

Leucocyte 13,79 4,7-11,3 103/µl
Haemoglobin 16,5 11,4 – 15,1 gr/dl
Hematocrit 47,9 38 - 42 %
Platelet 317 142-424 103/µl
MCV/MCH 90,5/31,2 80-93/27-31
Diff Count 0/0,2/92,4/3,6/3,8 0-4/0-1/5-67/25-33/2-5
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 patient blood gas analysis show a acid-base disturbance process which is Metabolic acidosis
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”
Kesimpulan : Sinus rhythm dengan
heart rate 93 bpm, LVH
CHEST XRAY – 28/07/16

• AP position, symetric
• Trachea in the middle, bone normal

• Aortic classification (+)

• Right and left phrenico-costalis angle sharp
• Right and left hemidiaphragm are domeshape

• Lung: Normal
• Cor: CTR: 65 %, cardiac waist (-), apex embedded
• Conclusion: Cardiomegaly
 Head ct-scan – 28/07/16
• Hyperdens lesions with perifocal edema in left subcortical lobe,
size 51,3 x 54,7 x 63 mm press the left ventricular region
• Hyperdens lesions of subarachnoid space on right frontal sulcii,
right temporal region, anterior falk cerebri, and left prepontin
cysterna region
• Hyperdens lesion filling the posterior cornu of left and right
lateral ventricles
• Sulcii, sylvii fissura are narrowing
• Widening right ventricle with asymmetrical narrowed cysterna
system
• Midline shift to the right 9,3 mm
Conclusion :
- SAH of frontal right lobe, left temporal, anterior falk cerebri,
and left prepontin cysterna with intraventricular hemorrhage in
left and right lateral ventricle
- Intracranial hemorrhage of left frontal lobe with volume 91,9 cc
- Cerebral edema with right herniation with 9,3 mm
TREATMENT

• Head up 30°
• 02 10 lpm via NRBM
• IVFD NaCl 0,9% 20 tpm
• Ranitidine 50 mg IV
• Ondancentron 4 mg IV
• Foley catheter insertion
• Nasogastric tube insertion
• If there is sign of increased ICP, give IV mannitol with dose 1 g/kgBB, in patient with 60 kg BB= 60 g
mannitol. Infuse with 20 % mannitol 200 g/500 ml 150 ml in 30-60 minutes
DISCUSSION

1. Woman, 63 yo, patient suffered decrease of consciousness since 2 hours before admission. Before
that there was episode of severe headache accompanied by nausea and vomiting, 7 hours before
admission. She has history of uncontrolled chronic hypertension since 8 years ago.
2. Physical examination: BP 160/130 mmHg (3.30 p.m) become 165/85 mmHg (6.00 p.m), HR 93 bpm
(3.30 p.m) become 80 bpm (6.00 p.m) , RR 22 tpm (3.30 p.m) become 24 tpm (6.00 pm), Tax 36,60C.
3. Chest X-ray : cardiomegaly, Head CT scan : SAH and cerebral edema, ECG : sinus rhythm HR 93 bpm
with LVH
4. Treatment: O2 10 lpm via NRBM, IV line IVFD NaCl 0.9% 20 tpm, Foley catheter and NGT insertion, if
needed IV mannitol with dose 1 g/kgBB, in patient with 60 kg BB= 60 g mannitol. Infuse with 20 %
mannitol 200 g/500 ml 150 ml in 30-60 minutes

Based on data from anamnesis, primary and secondary survey, we can conclude the patient
suffered Altered Mental State due to Subarachnoidal Hemorrhage
 Definition
• An alteration in mental status refers to general changes in
brain function, such as confusion, amnesia (memory loss), loss
of alertness, loss of orientation (not cognizant 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)

21
CLASSIFICATION (Tom Morrissey,2008)22

• Three common broad classifications of AMS include delirium, dementia and psychosis
ETIOLOGY 23

(Tom Morrissey, 2008)

 24

CLINICAL SIGNS & SYMPTOMS

(World J. Emerg. Med., Medical College Hospital, Chinese Academy,

China, 2012)
HOW TO EVALUATE THE LEVEL OF CONSCIOUSNESS

 AVPU (alert, verbal, pain, unresponsive)

 Quantitative : GCS
 Qualitative :
1. Compos Mentis
2. Apatis
3. Delirium
4. Somnolen
5. Stupor
6. Coma
 Level of Consciousness (Qualitative)
• Hyper-alert : heightened arousal with increased sensitivity to immediate surroundings.
Hyper-alert patients can be verbally and physically threatening, restless and/or
aggressive.
• Confused : disorientated, bewildered, and having difficulty following commands.
• Delirious : disorientated, restless, hallucinating, sometimes delutional.
• Somnolent : sleepy, responding to stimuli only with incoherent mumbles or
disorganized movements.
• Letargic : reduced level of alertness with decreased interest in the surrounding
environment.
• Obtunded : similar to lethargy; the patient has a lessened interest in the surrounding
environment.
• Stuporous : profoundly reduced alertness and requiring continious noxious stimuli for
arousal.
• Comatose : state of deep, unarousable, sustained unconsciousness
DETERMINE STRUCTURAL OR NON STRUCTURAL 28

CAUSES OF AMS

Non structural causes Structural causes

Empty pill container Complained of headache to family/friends prior
AMS
Medical diseases, e.g epilepsy, liver disease, diabetes, History of brain tumor
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 cause
- Respiration rate and pupil size
- Chronic organ failure sign
29
 Structural cause Toxic/metabolic cause

Head trauma
Intracranial hemorhage Afebrile
Febrile:
Non head trauma : Poisons
- Cerebral abcess
- Intracranial hemorrhage - Drug overdose; Opioid,
- Meningitis
- Subarachnoid hemorrhage BZD,barbiturate,TCA,ketamine
- Encephalitis
- Brainstem stroke - Alcohol intoxication
- Cerebral malaria
- Cerebellar stroke - Wernicke’s encephalopathy
- Bacteraemia
- Cerebral tumor - Carbon monoxide
- Septicaemia
Metabolic
- UTI in elderly
- hypoglicemia, cerebral hypoperfusion,
- Heat stroke
hypercarbia, diabetic coma,
- Thyroid crisis
myxoedema 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) 30

(Xiao et al, World Journal of Emergency Medicine vol.3 no.4, 2012)
 SUBARACHNOID
32 HEMORRHAGE

Sign and Symptoms

1. Sudden onset of severe headache
2. Nausea and/or vomiting from increased ICP
3. Symptoms of meningeal irritation, including nuchal rigidity and
neck stiffness, back pain, and bilateral leg pain
4. Focal neurologic deficits may also occur
5. Loss/decrease of consciousness

Diagnosis
1. Clinical sign & symptoms
2. CT scan ( e.g hydrocephalus)
3. Lumbar puncture (xantochromic)
4. Cerebral angiography
5. MRI (Tibor Becske, 2015)
 INCREASED INTRACRANIAL PRESSURE

• SAH can increased intracranial pressure which is caused hydrocephalus by 2

mechanisms: obstruction of CSF pathways and blockage of arachnoid
granulations by scarring
• Intractable elevated ICP can lead to death or devastating neurological damage either
by reducing cerebral perfusion pressure (CPP)[6] and causing cerebral ischemia
or by compressing and causing herniation of the brainstem or other vital
structures.

(Tibor Becske, 2015)

33
34

(Normal value of ICP 7-15 mmHg)

Triad Cushing of Elevated Intracranial Pressure

• Irregular respirations (caused by impaired brainstem function)
• Bradycardia
• Systolic hypertension (Widening Pulse Pressure)
(Gaurav, 2015)
IN THE PATIENT..

Physical examination:
1. BP 160/130 mmHg (3.30 p.m) become 165/85 mmHg (6.00 p.m) High sistolic blood
pressure
2. HR 93 bpm (3.30 p.m) become 80 bpm (6.00 p.m) Relative bradycardia
3. RR 22 tpm (3.30 p.m) become 24 tpm (6.00 pm) Takipneu with irregular breathing
Based on the physical examination fullfill the triad cushing of the elevated
intracranial pressure so the planning management is to decrease the intracranial pressure
Rodon, 2011. Altered Mental Status in Urgent Care Patient. The Journal of
Urgent Care Medicine 2011 Vol 6 No. 3
 37
MANAGEMENT AMS

• Due to structural causes (based on theory)

Treatment of this patient, include :
1. Initial Management : ABC 1. Head up 30°
2. Give suplemental oxygen to maintain SpO2 of 2. 02 10 lpm via NRBM
at least 95 % 3. IVFD NaCl 0,9% 20 tpm
4. Ranitidine 50 mg IV
3. Start IV at slow rate 5. Ondancentron 4 mg IV
4. Perform head CT scan 6. Foley catheter insertion
5. Lower intracranial pressure if indicated, by 7. Nasogastric tube insertion
8. If there is sign of increased ICP, give IV mannitol with
a. Controlled ventilation : work fastest dose 1 g/kgBB, in patient with 60 kg BB= 60 g mannitol.
b. IV mannitol in conjunction with neurosurgical Infuse with 20 % mannitol 200 g/500 ml 150 ml in 30-
result. Dose is 1g/kg body weight 60 minutes
(Peter Manning & Goh Ee ling, 2015)
WORKING DIAGNOSE

From primary survey and secondary survey wich include anamnesis, physical
examination and also further diagnostic evaluation, we can conclude that diagnose patient
was :
1. AMS dt SAH
DISPOSITION  Neurologic Departement
LESSON LEARNT

 Alteration in mental status refers to general changes in brain function, defects

in judgment or thought, unusual or strange behavior, poor regulation of emotions,
and disruptions in perception, psychomotor skills, and behavior.
 Diagnose of AMS can be finding on clinical signs and symptoms, examination
qualitative or quantitative the level of consciousness, define the structural or
non structural causes to chose the additional workup based on the etiology
with head CT scan, MRI, etc.
 The management of AMS is divided in to initial assesment include primary and
secondary survey) and definitive care based on the etiology.