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Revisi 1 PPT Death Case SAH + PE.pptx
1. Subarachnoid Hemorrhage Complicated by
Acute Pulmonary Embolism
Presented by:
dr. Renard Christian
Supervisor:
dr. Pinto Desti Ramadhoni, Sp.S (K), FINA
Dr. Erwin Sukandi, Sp.PD-KKV, FINASIM
NEUROLOGY DEPARTMENT
MOH. HOESIN CENTRAL GENERAL HOSPITAL PALEMBANG
MEDICAL FACULTY OF SRIWIJAYA UNIVERSITY PALEMBANG
2022
2. Introduction
2
STROKE
2013
10.3 million new cases
6.5 million death cases
113 million cases
disability due to stroke
Divided into:
1. Non Hemorrhage
2. Hemorrhage
Definition
Intracerebral
Hemorrhage
Subarachnoid
Hemorrhage
Bleeding in the subarachnoid space
caused by ruptured intracranial
aneurysm
Incidence 2-22 million/100.000
people/year
High mortality 34-52% (Hunt and
Hess IV & V)
Complication thromboembolic
PE (2%) life threatening
Our case ?
3. Case study
• Identity
• Chief complaint:
– Sudden loss of consciousness.
3
Patient Identity
Name Mrs. S
Date of birth (age) June 11th 1964 (58 y.o)
Address Pangkalan Balai, Banyuasin
Medical record 0001236458
Admission date Desember 10th 2022
4. Case study…
4
• Sudden unconsciousness
during activity
• Headache (+)
• Projectile vomit (+)
• Seizure (-)
• Asymmetrical corners of the
mouth
• Language disorders can not
be assessed
• Communication disorders
can not be assessed
6 Days before admission Historical illness:
• Hypertension (5 years ago) uncontrolled
• Diabetes mellitus (-)
• Cardiac problem (-)
• Head trauma (-)
• Smoking (-)
• Previous stroke (-)
Medical history:
• Tranexamic acid 4x1 grams i.v
• Ceftriaxone 2x1 grams i.v
• Mannitol 4x125 cc i.v
• Omeprazole 1x40 mg i.v
• Glaucon 3x500 mg p.o
• Nimotop 4x60 mg p.o
This disease is experienced for the 1st time.
5. • General examination
5
Sensorium E4M5V4
Blood pressure 130/80 mmHg
Heart rate 106 beat / minutes
Respiratory rate 22 beat / minute
Temperature 36.8 ºC
Oxygen saturation 99%
Body mass index Normal range
Eye Icteric -/-, anemic -/-
Neck lymph node enlargement (-), torticollis (-)
Cardiac Normal heart sound, regular, murmur (-), gallop (-)
Pulmonary Vesicular +/+, wheezing -/-, rhonchi -/-
Case study…
6. • Neurological examination
6
Cranial nerve examination
N.I Can’t be assessed
N.II Vision : Can’t be assessed
Funduscopic: well defined, redness, c/d = 0,3, A/V = 2/3
N.III Pupillary : Round, middle, diameters 3mm / 3 mm, light reflex (+/+)
N.III, IV, VI The position of the eyeball in the middle, conjugate deviation (-)
N.V Cornea reflex (+)
N.VII Symmetrical forehead crease
Flat left nasolabial fold, asymmetrical corners of the mouth
N.VIII Nystagmus (-)
N.IX, X Vomit reflex (+)
N.XI Can’t be assessed
N.XII Can’t be assessed
Case study…
7. 7
Motor function Right arm Left arm Right leg Left leg
Movement Lateralization (-)
Strength
Tone ↑ ↑ ↑ ↑
Clonus (-) (-)
physiological reflex ↑ ↑ ↑ ↑
pathological reflex (-) (-) Babinsky (+) Babinsky (+)
Sensory function Can’t be assessed
Higher cortical function Can’t be assessed
Vegetative function Can’t be assessed
Meningeal sign Nuchal rigidity (+), Lasseque (+/+), Kerniq (+/+),
Symphisis sign (+)
Abnormal movement (-)
Gait and balance Can’t be assessed
Case study…
25. • Definition
– SAH acute bleeding in the subarachnoid cavity between
pia mater and arachnoid mater (part of membrane that covers
the brain/meninges).10,11
• Anatomy12
– Meninges: a system of membranes that line CNS
– Composed of elastic collagen, fibrin and CSF
– 3 layers dura mater, arachnoid and pia mater.
25
10. Gofir A. Tatalaksana Stroke Dan Penyakit Vaskuler Lain. Vol. 1. Gadjah Mada University Press; 2020. 103–122
11. Aninditha TW. Buku Ajar Neurologi. Pertama. Jakarta: Departemen Neurologi FK UI; 2017.
12. Baehr M, Frotscher M. I Thieme. Duus’ Topical Diagnosis in Neurology Anatomy.
Literature
review…
26. • Epidemiology1,4,5
– Incidence 2-22 cases/100,000/year
– 60% 40-60 y.o
– Indonesian stroke registry (2012-2014) 181 of 5411 stroke
patients/± 3.3% of total stroke patients.
– Estimated 30-day mortality rate is 35%
• Etiology13
26
Etiology Percentage (%)
Aneurysm rupture 85
Non-aneurysmal permesenphalic haemorrhage 10
1. Venketasubramanian N, Yoon BW, Pandian J, Navarro JC. Stroke epidemiology in south, east, and south-east asia: A review. Vol. 19, Journal of Stroke.
Korean Stroke Society; 2017. p. 286–94.
4. Petridis AK, Kamp MA, Cornelius JF, Beez T, Beseoglu K, Turowski B, et al. Aneurysmal subarachnoid hemorrhage-diagnosis and treatment. Vol. 114,
Deutsches Arzteblatt International. Deutscher Arzte-Verlag GmbH; 2017. p. 226–35.
5. Harris S, Kurniawan M, Rasyid A, Mesiano T, Hidayat R. Cerebral small vessel disease in Indonesia: Lacunar infarction study from Indonesian Stroke
Registry 2012–2014. SAGE Open Medicine. 2018 Jan 1;6:205031211878431.
13. Suarez JI, Tarr RW, Selman WR. Aneurysmal Subarachnoid Hemorrhage. 2006.
Literature
review…
27. • Pathophysiology3
27
3. Reis C, Ho WM, Akyol O, Chen S, Applegate R, Zhang JH. Pathophysiology of Subarachnoid Hemorrhage, Early Brain Injury, and Delayed
Cerebral Ischemia. In: Primer on Cerebrovascular Diseases: Second Edition. Elsevier Inc.; 2017. p. 125–30.
Literature
review…
28. • Clinical manifestations14
– Most common Headache the worst headache ever
experienced, suddenly and lasting at most within an hour
– Nausea and vomiting (77%), loss of consciousness (53%),
meningismus (35%), focal deficits (10%), and Terson's syndrome
(vitreous haemorrhage associated with SAH) (40%)
• Diagnosis6
– Severe and sudden onset/rapidly increasing headache
“thunderclap headache”
– Symptoms syncope, vomiting, neck pain, and seizures.
– Focal neurologic deficits, photophobia, diplopia, meningismus,
and/or retinal hemorrhages 50% of patients the neurologic
examination is normal.
28
6. Marcolini E, Hine J. Approach to the diagnosis and management of subarachnoid hemorrhage. Vol. 20, Western Journal of Emergency Medicine.
eScholarship; 2019. p. 203– 11.
14. Rouanet C, Silva GS. Aneurysmal subarachnoid hemorrhage: current concepts and updates. Vol. 77, Arquivos de neuro-psiquiatria. NLM (Medline); 2019.
p. 806–14.
Literature
review…
29. – Hunt and Hess Scale
– World Federation of Neurosurgical Societies (WFNS) Scale
29
Literature
review…
30. Algorithm approach to
subarachnoid hemorrhage4
30
4. Petridis AK, Kamp MA, Cornelius JF, Beez T, Beseoglu K,
Turowski B, et al. Aneurysmal subarachnoid hemorrhage-
diagnosis and treatment. Vol. 114, Deutsches Arzteblatt
International. Deutscher Arzte-Verlag GmbH; 2017. p. 226–
35.
Literature
review…
31. • Complications
– Acute complications (Day 0-3)
• Rebleeding
– Serious complication 1st 3 days after initial bleeding (7-22%)
• Acute hydrocephalus
– Sudden dilatation of ventricular system obstruction of CSF
flow caused by degradation products of blood as it enters the
ventricles
• Acute ischemic lesion
– Rare
– Pathophysiology unclear: diffuse cortical ischemic injury
death within hours of subarachnoid hemorrhage
31
19. Danière F, Gascou G, Menjot De Champfleur N, Machi P, Leboucq N, Riquelme C, et al. Complications and follow up of subarachnoid hemorrhages. Vol.
96, Diagnostic and Interventional Imaging. Elsevier Masson SAS; 2015. p. 677–86.
20. Connolly ES, Rabinstein AA, Carhuapoma JR, Derdeyn CP, Dion J, Higashida RT, et al. Guidelines for the management of aneurysmal subarachnoid
hemorrhage: A guideline for healthcare professionals from the american heart association/american stroke association. Vol. 43, Stroke. 2012. p. 1711–37.
Literature
review…
32. • Complications
– Subacute complications (Day 3-30)
• Vasospasm19
– Most common
– Day 4-15, but cases of late vasospasm have also been
reported
– Extravascular blood clots degradation and lysis in the
cerebral fluid vasoactive mediators cerebral
vasoconstriction decreased cerebral blood flow
– The danger sign worsening of the focal neurologic
deficit (3rd day after onset)
– The presence of fever in the absence of other clues to
infection, or sweating, agitation, or confusion should also
suggest vasospasm.
32
19. Danière F, Gascou G, Menjot De Champfleur N, Machi P, Leboucq N, Riquelme C, et al. Complications and follow up of subarachnoid hemorrhages. Vol.
96, Diagnostic and Interventional Imaging. Elsevier Masson SAS; 2015. p. 677–86.
Literature
review…
33. • Complications
– Chronic complications (After day 30)
• Chronic hydrocephalus19
– Occurs late after the initial subarachnoid hemorrhage
– Classic symptoms difficulty walking, sphincter and
cognitive impairment, disorientation and confusion.
– Due to partitioning in the arachnoid space prevents
normal reabsorption of cerebrospinal fluid and causes
dilatation of the ventricular system.
33
19. Danière F, Gascou G, Menjot De Champfleur N, Machi P, Leboucq N, Riquelme C, et al. Complications and follow up of subarachnoid hemorrhages. Vol.
96, Diagnostic and Interventional Imaging. Elsevier Masson SAS; 2015. p. 677–86.
Literature
review…
34. • Complications
– Systemic complications
• Cardiac complication22
– SAH cardiac function (direct/indirect)
– Stimulation of the hypothalamus, ventral hippocampus,
medial amygdala, and reticular formation various
morphological changes and ECG rhythms.
– Stimulation irritation by blood/ICP
– The catecholamine surge can affect the myocardium
through a variety of mechanisms leading to cardiac
dysfunction
34
22. Garg R, Bar B. Systemic Complications Following Aneurysmal Subarachnoid Hemorrhage. Vol. 17, Current Neurology and Neuroscience Reports.
Current Medicine Group LLC 1; 2017.
Literature
review…
35. • Complications
– Systemic complications
• Pulmonary complications
– 22%
– Nosocomial pneumonia, aspiration pneumonia, neurogenic
pulmonary edema, and pulmonary embolism (PE) with an
incidence of < 1% (ischemic and hemorrhagic stroke).
– One of the more common pulmonary complications of SAH
than other types of stroke is neurogenic pulmonary edema
(NPE).
– Clinical presentation of NPE non-specific signs of respiratory
distress: tachypnea, dyspnea, tachycardia, cyanosis, frothy
sputum, hypotension.
35
22. Garg R, Bar B. Systemic Complications Following Aneurysmal Subarachnoid Hemorrhage. Vol. 17, Current Neurology and Neuroscience Reports.
Current Medicine Group LLC 1; 2017.
Literature
review…
36. • Complications
– Systemic complications
• Anemia
– Etiology: blood loss during surgery, SIRS, and frequent
phlebotomy.
– Guidelines for the Neurocritical Care Society (NCS)
recommend RBC transfusion to maintain a Hb
concentration >8-10 g/dL
• Hyponatremia
– Most common electrolyte abnormality after SAH
– Primarily caused by the inappropriate antidiuretic
hormone (SIADH) syndrome, cerebral salt wasting
(CSW), or acute glucocorticoid deficiency.
36
22. Garg R, Bar B. Systemic Complications Following Aneurysmal Subarachnoid Hemorrhage. Vol. 17, Current Neurology and Neuroscience Reports.
Current Medicine Group LLC 1; 2017.
Literature
review…
37. • Pulmonary embolism
– Venous thromboembolism (VTE) : deep vein thrombosis (DVT)
and pulmonary embolism (PE) fatal medical complications
following ICH and SAH.23
– Incidence (< 1% ) 23/100,000 population mortality rate
(15%) cardiovascular emergency.24
– Risk factors: elderly, high NIHSS score, hemiparesis, immobility,
female, atrial fibrillation, intravenous or intra-arterial tissue
plasminogen activator (tPA), and length of hospitalization.24
37
23. Cohen AT, Tapson VF, Bergmann J-F, Goldhaber SZ, Kakkar AK, Deslandes B, et al. Venous thromboembolism risk and prophylaxis in the acute hospital
care setting (ENDORSE study): a multinational cross-sectional study. Vol. 371. 2008.
24. Lee SH, Jeong WJ, Choi SK, Kwun BD. Deep Vein Thrombosis and Pulmonary Embolism following Hemorrhagic Stroke. Journal of Neurointensive Care.
2018 Oct 10;1(1):20–4.
Literature
review…
38. • Pulmonary embolism
– Predisposing factors27
38
27. Torbicki A, Perrier A, Konstantinides S, Agnelli G, Galiè N, Pruszczyk P, et al. Guidelines on the diagnosis and management of acute pulmonary
embolism. Vol. 29, European Heart Journal. Oxford University Press; 2008. p. 2276–315.
Strong risk factors Moderate risk factor Weak risk factors
Lower extremity fracture
Hospitalization for heart failure/atrial
fibrillation/flutter (within the previous 3
months)
Hip/knee replacement
Major trauma
Myocardial infarction (within the
previous 3 months)
Previous VTE
Spinal injury
Knee arthroscopic surgery
Autoimmune disease
Blood transfusion
Central venous catheter
Intravenous catheter and leads
Chemotherapy
Congestive heart failure and respiratory
failure
Erythropoiesis-stimulating agents
Hormone replacement therapy (depending
on formulation)
In vitro fertilization
Infections (especially pneumonia, UTI and
HIV)
Inflammatory bowel disease
Cancer (high risk of metastases)
Paralytic stroke
Superficial vein thrombosis
thrombophilia
Bed rest > 3 days
Diabetes mellitus
Arterial hypertension
Immobility due to sitting (in car or
air travel)
Age increase
Laparoscopic surgery (such as
cholecystectomy)
Obesity
Pregnancy
Varicose veins
Literature
review…
39. • Pulmonary embolism
– Patophysiology27
• Virchow’s triad
• Emboli increase the resistance and pressure in the pulmonary
arteries release vasoconstrictor compounds, platelet aggregation,
and mast cells.
39
27. Torbicki A, Perrier A, Konstantinides S, Agnelli G, Galiè N, Pruszczyk P, et al. Guidelines on the diagnosis and management of acute pulmonary
embolism. Vol. 29, European Heart Journal. Oxford University Press; 2008. p. 2276–315.
Literature
review…
40. • Pulmonary embolism
– Clinical manifestation
• Signs and symptoms non-specific and can be a
manifestation of other diseases: myocardial infarction and
pneumonia.27
40
27. Torbicki A, Perrier A, Konstantinides S, Agnelli G, Galiè N, Pruszczyk P, et al. Guidelines on the diagnosis and management of acute pulmonary
embolism. Vol. 29, European Heart Journal. Oxford University Press; 2008. p. 2276–315.
Symptom Frequency (%)
Dyspnea 73
Pleuritic pain 66
Cough 37
Swelling in the lower limbs 33
Coughing up blood 13
Wheezing 6
Sign Frequency (%)
Respiratory rate more than 20 times per minute 70
Ronki 51
Heart rate more than 100 beats per minute 30
3 and 4 heart sounds (gallops) 26
Cyanosis 11
Temperature over 38.5oC 7
Literature
review…
41. • Pulmonary embolism
– Clinical manifestation
41
29. Konstantinides S v., Meyer G, Galié N, Simon R Gibbs J, Aboyans V, Ageno W, et al. 2019 ESC Guidelines for the diagnosis and management of acute
pulmonary embolism developed in collaboration with the European Respiratory Society (ERS). Vol. 54, European Respiratory Journal. European
Respiratory Society; 2019.
Variable Score
Clinical signs and symptoms of deep vein thrombosis 3.0
Other differential diagnoses have a lower probability compared to pulmonary embolism 3.0
Pulse more than 100 beats/minute 1.5
Immobilization or surgery in the last 4 weeks 1.5
Previous history of DVT or pulmonary embolism 1.5
Hemoptysis 1.0
Cancer (received treatment in the last 6 months or received palliative management) 1.0
Well’s Score29
0 – 1 : low probability
2 – 6 : medium possibility
> 6 : high probability
Variable Score
> 65 years old 1
History of PE or DVT 3
Surgery or fracture in the last 1 month 2
Active malignancy 2
Unilateral pain in the lower leg 3
Hemoptysis 2
Pain on palpation of the deep veins of the lower leg accompanied by unilateral edema 4
Pulse 75 to 94 times per minute 3
Pulse more than 95 beats per minute 5
0 – 3: low probability (< 8%)
4 – 10: moderate probability (+ 28%)
>10: high probability (+ 74%)
Geneva Score29
and
Literature
review…
42. • Pulmonary embolism
– Diagnosis27,29
• Anamnesis and PE
• Lab: assess progress of therapy and other possible diagnosis (increase in
plasma levels of D-dimer)
• CXR examination pleural effusion /atelectasis
• ECG usually normal in mild-moderate but in severe:
– S1Q3T3
– P pulmonale
– RBBB
– Right ventricular strain with T wave inversion in leads V1 to V4
– Supraventricular arrhythmias or sinus tachycardia
• Ventilation-perfusion scintigraphy (V/Q scan)
• Pulmonary angiogram Gold standard
• CT sensitivity (70%) and specificity (90%)
• Transthoracic echocardiography
• Cardiac biomarkers estimate the prognosis
42
27. Torbicki A, Perrier A, Konstantinides S, Agnelli G, Galiè N, Pruszczyk P, et al. Guidelines on the diagnosis and management of acute pulmonary
embolism. Vol. 29, European Heart Journal. Oxford University Press; 2008. p. 2276–315.
29. Konstantinides S v., Meyer G, Galié N, Simon R Gibbs J, Aboyans V, Ageno W, et al. 2019 ESC Guidelines for the diagnosis and management of acute
pulmonary embolism developed in collaboration with the European Respiratory Society (ERS). Vol. 54, European Respiratory Journal. European
Respiratory Society; 2019.
Literature
review…
43. • Pulmonary embolism
– Management29
• Respiratory and hemodynamic stabilizatin, thrombolysis, embolectomy,
anticoagulation.
• Thrombolytic therapy open thromboembolic plugs and (+) effect on
hemodynamic parameters.
• Contraindications to the administration of fibrinolytic therapy:
43
29. Konstantinides S v., Meyer G, Galié N, Simon R Gibbs J, Aboyans V, Ageno W, et al. 2019 ESC Guidelines for the diagnosis and management of acute
pulmonary embolism developed in collaboration with the European Respiratory Society (ERS). Vol. 54, European Respiratory Journal. European
Respiratory Society; 2019.
Absolute contraindication Relative contraindications
Hemorrhagic stroke or stroke with unknown cause Transient ischemic attack within the last 6 months
Ischemic stroke in the last 6 months Use of oral anticoagulant therapy
Damage to the central nervous system or neoplasm Pregnancy or condition 1 week post partum
Major trauma, surgery or trauma to the head within the last 3 weeks Refractory hypertension, with systolic blood pressure >180 mmHg
Gastrointestinal bleeding within the last 1 month Advanced stage liver disease
Active bleeding Infective endocarditis
Peptic ulceractive
Literature
review…
44. • SAH Management
– Stabilization
– Rebleeding prevention
– Surgical and endovascular management of aneurysms.
– Management of vasospasm and delayed cerebral ischemia
– Hydrocephalus management
– Seizure management
– Management of complications
44
Literature
review…
45. Case Analysis
45
Anamnesis:
• sudden decrease of
consciousness
• severe headaches
before
• Projectile vomit (+)
• asymmetrical
corners of the mouth
• Risk factor:
Hypertension
uncontrolled
Physical &
Neurological exam:
• Sens: E4M5V4
• BP: 130/80 mmHg
• HR: 106x/min
• Spastic type
quadriparesis
• Central type left
facial nerve
paresis
• Meningeal sign (+)
Differential diagnosis
(Sudden onset loss of consciousness)
Traumatic brain
injury
• No Traumatic
history
• No sign of head
or neck trauma
exclude
Drug poisoning • No history of
taking drugs
exclude
Vascular problems • Severe
Headache
• Meningeal sign
(+)
• Sirriraj score
(+2.5)
Suspect.
Hemorrhagic stroke
(Subarachnoid
Hemorrhage)
Non-Contrast
Head CT
(AHA/ASA, Class I, level
of evidence B)
Hyperdense lesions filled the
interhemispheric falx, sulci, Sylvian
cisterns, suprasellar cisterns,
ambient cisterns with widened gyri,
suggests a Fisher 3 subarachnoid
hemorrhage
Hunt and Hess scale (AHA/ASA Class I, level of evidence B)
58-year-old woman treated in neurology dept. Moh. Hoesin General Hospital
46. 46
Subarachnoid
Hemorrhage
Management
in Stroke Unit
(AHA/ASA, Class I, level of
evidence A)
Treatment Aim Recommendation Patient
Head elevation 30º Lowering ICP &
increase perfusion
the benefits are still
not clear
✅
Oxygenation Maintain O2
saturation
AHA/ASA Class I,
Level of evidence C
✅
Sodium Chloride
0.9% 20 drops/min
Maintain
euvolemia &
prevent DCI
AHA/ASA Class I,
Level of evidence B
✅
Tranexamic acid 4x1
grams intravenous
Reduce risk of
rebleeding
AHA/ASA Class IIa,
Level of evidence B
✅
Nimodipine 4x60 mg Improve
neurological
outcome
AHA/ASA Class I,
Level of evidence A
✅
Paracetamol 3x1
grams intravenous
Pain management
& control of fever
AHA/ASA Class IIa,
Level of evidence B
✅
DSA with 3-
dimentional rotation
angiography
Detection
aneurysm & plan
for treatment
AHA/ASA Class I,
Level of evidence B
✅
2 days of treatment
• Sudden severe shortness of
breath
• decreased oxygen
saturation
• Rhonchi +/+
• Sens: E4M5V4
• No new neurological deficits
Acute pulmonary edema
Anesthesiology
Internal dept.
Pro intubation
ETT
Family refuse
intubation
Furosemide
(ACC/AHA/HRS Class I,
Level of evidence B)
to achieve
euvolemic status
(dry and warm)
improvement in shortness of breath and an increase in
peripheral oxygen saturation (only lasted a few hours)
Next day
Case
analysis…
47. 47
• Shortness of breath
• SpO2: 96%
• Rhonchi -/-
• Sens: E4M5V4
• No new neurological deficits
Next day
Echocardiography:
• LVH preserved EF
• Right ventricular
dilatation
• Mild-moderate tricuspid
valve regurgitation
ECG:
• S wave in lead I, a
Q wave in lead III
and an inversion of
the T wave in lead
III
CXR
• Cardiomegaly
• Pulmonary
hypertension
Blood Gas Analysis
pH 7.376
pCO2 28.3 mmHg
pO2 63.4 mmHg
HCO3 16.8 mmol/L
Hemostasis function
Fibrinogen 648 mg/dL
D-dimer 5.51
Suspect pulmonary
embolism
Case
analysis…
48. • Pulmonary embolism
– Clinical manifestation
48
27. Torbicki A, Perrier A, Konstantinides S, Agnelli G, Galiè N, Pruszczyk P, et al. Guidelines on the diagnosis and management of acute pulmonary
embolism. Vol. 29, European Heart Journal. Oxford University Press; 2008. p. 2276–315.
Symptom Frequency (%)
Dyspnea 73
Pleuritic pain 66
Cough 37
Swelling in the lower limbs 33
Coughing up blood 13
Wheezing 6
Sign Frequency (%)
RR > 20 times/minute 70
Rhonhi 51
HR > 100 beats/minute 30
3 and 4 heart sounds (gallops) 26
Cyanosis 11
Temperature over 38.5oC 7
Case
analysis…
49. • Pulmonary embolism
– Clinical manifestation
49
29. Konstantinides S v., Meyer G, Galié N, Simon R Gibbs J, Aboyans V, Ageno W, et al. 2019 ESC Guidelines for the diagnosis and management of acute
pulmonary embolism developed in collaboration with the European Respiratory Society (ERS). Vol. 54, European Respiratory Journal. European
Respiratory Society; 2019.
Variable Score
Clinical signs and symptoms of deep vein thrombosis 3.0
Other differential diagnoses have a lower probability compared to pulmonary embolism 3.0
Pulse more than 100 beats per minute 1.5
Immobilization or surgery in the last 4 weeks 1.5
Previous history of DVT or pulmonary embolism 1.5
Hemoptysis 1.0
Cancer (received treatment in the last 6 months or received palliative management) 1.0
Well’s Score29
0 – 1 : low probability
2 – 6 : medium possibility
> 6 : high probability
Variable Score
Over 65 years old 1
History of pulmonary embolism or DVT 3
Surgery or fracture in the last 1 month 2
Active malignancy 2
Unilateral pain in the lower leg 3
Hemoptysis 2
Pain on palpation of the deep veins of the lower leg accompanied by unilateral edema 4
Pulse 75 to 94 times per minute 3
Pulse more than 95 beats per minute 5
0 – 3: low probability (< 8%)
4 – 10: moderate probability (+ 28%)
>10: high probability (+ 74%)
Geneva Score29
and
Case
analysis…
50. 50
Algorithm for treating pulmonary embolism with hemodynamic disturbances.
Management respiratory and hemodynamic stabilization, thrombolysis, embolectomy, anticoagulant.
Case
analysis…
suspected hemodynamically unstable pulmonary embolism
echocardiography
Left ventricle disfunction
Computed Tomography Pulmonary Angiography (CTPA)
Yes
No
CTPA available
No Yes
CTPA
Positive Negative
Look for other causes
of hemodynamic
disorders
high risk
pulmonary
embolism
therapy
Look for other causes
of hemodynamic
disorders
51. • Systemic thrombolysis effective with satisfactory hemodynamic
recovery, but contraindication with intracranial hemorrhage.
• This patient has SAH: contraindication to systemic thrombolytic
therapy.
• Patients with contraindications to thrombolysis or systemic
thrombolysis fails to improve hemodynamic status surgical
embolectomy or CDT (if available)
• Wei-Chieh Lee et al (2018) : combined intravenous unfractionated
heparin (UFH) and non-vitamin K oral anticoagulant (NOAC)
treatment in life-threatening PE with intracranial hemorrhage.
(systemic thrombolysis cannot be given because of intracranial
bleeding UFH : control the therapeutic dose and convert the
anticoagulant effect if massive bleeding occurs)
51
Case
analysis…
52. • Giving anticoagulation after hemorrhagic stroke therapeutic dilemma.
• Fong et al.: increased intracerebral hemorrhage mortality was
associated with patients taking warfarin for atrial fibrillation.
• Risk of recurrence of intracerebral hemorrhage 2%-4%/patient/year,
risk of severe bleeding 2%-3%/year and may be higher in the 1st month.
• AHA: 4 weeks after ICH to initiate or continue anticoagulation.
• Zhou et al. no definite timetable to resume anticoagulant (further
studies are needed)
52
Case
analysis…
53. • The cause of death: right ventricular failure (pulmonary artery
obstruction) intraventricular septal compression and tricuspid
valve regurgitation reduced left ventricular filling systemic
cardiac output decrease and reduce coronary perfusion
myocardial infarction cardiogenic shock circulatory failure and
death
• PE as complications of SAH and family refusal to respiratory and
airway stabilization non-optimal management of the patient.
53
Case
analysis…
54. Conclusion
• We report a case report of a 58-year-old woman with sudden loss of
consciousness due to subarachnoid hemorrhage. During treatment,
the patient experienced pulmonary embolism as a complications of
systemic subarachnoid hemorrhage which caused hemodynamic
instability. The presence of pulmonary embolism in subarachnoid
hemorrhage and family refusal to respiratory and airway stabilization
causes non-optimal management of the patient to result in cardio-
pulmonary system failure and ends in death.
54
Thank you for dr. afriani neurologist for the opportunity.
First of all, I would like to thank dr. pinto desti ramadhoni neurologist consultant and dr. erwin sukandi internist consultant cardiology FINASIM as my mentor
I also thank dr. theresia christin neurologist consultant and dr. Hj. Sri Handayani neurologist consultant as the examiner on this occasion.
Thank you also to the doctors and colleagues who are willing to attend this scientific session
Stroke is defined as a condition in which there is a focal or global neurological deficit that occurs suddenly and lasts for 24 hours or more and/or causes death with no other cause other than vascular problem.
Stroke is still the leading cause of death and disability in many countries.
In 2013 it was reported that there were 25.7 million stroke survivors, 6.5 million stroke deaths, and 113 million stroke-related disabilities, as well as 10.3 million new cases.
In general, stroke can be divided into non-hemorrhagic and hemorrhagic strokes. Hemorrhagic stroke can be in the form of intracerebral hemorrhage or subarachnoid hemorrhage.
Subarachnoid hemorrhage (PSA) is a cerebrovascular disease that occurs due to rupture of an intracranial aneurysm, resulting in bleeding in the subarachnoid space.
incidence of acute subarachnoid hemorrhage is estimated to be 2-22 cases per 100,000 people per year, and 60% of all acute subarachnoid hemorrhages occur in people aged 40 to 60 years
The mortality rate for SAH is quite high, especially on the Hunt and Hess IV and V scale, reaching 34-52%.
Various complications and comorbidities that occur in subarachnoid hemorrhage greatly affect the outcome, including the mortality rate. Various complications can occur in SAH, either acute, sub acute, or chronic.
One of the systemic complications that are quite rare in SAH but can be life-threatening is the result of thromboembolic complications, including deep vein thrombosis, pulmonary embolism, and myocardial infarction.
Massive pulmonary embolism is a life-threatening condition and requires treatment with anticoagulants or even thrombolytic agents in high-risk cases.
This case report will describe a 58-year-old woman who was treated in the neurology department of RSMH because she experienced headaches and sudden loss of consciousness caused by subarachnoid hemorrhage. During treatment the patient suddenly experienced shortness of breath and suspected complications such as acute pulmonary embolism where anticoagulants and thrombolytic agents which are the treatment options for pulmonary embolism are contraindicated in acute bleeding episodes. Management of life-threatening pulmonary embolism in acute bleeding conditions is complicated in this case.
From physical examination, sensorium E4M5V4, blood pressure 130/80 mmHg, Heart rate 106 times per minute, respiratory rate 22 times per minute, body temperature 36.8C with a peripheral oxygen saturation of 99%.
On neurological examination, the left plicanasolabialis was flat,
there was no lateralization but there was an increase in muscle tone and physiological reflexes in all four extremities. Meningeal sign (+): nuchal rigidity, laseque +, kerniq +.
at 3 pm the patient’s has decreased of consciousness become E1M1Vopa and the patient was declared dead at 10 pm in front of the family
In the literature review we will discuss about subarachnoid hemorrhage and pulmonary embolism
SAH is acute bleeding in the subarachnoid cavity between pia mater and arachnoid mater (part of membrane that covers the brain/meninges).
The meninges are a system of membranes that line the central nervous system.
The meninges are composed of elastic collagen and fibrin and cerebrospinal fluid.
The meninges are divided into three layers, namely the dura mater, arachnoid and pia mater. The dura mater is also known as pachymeninges (hard membrane), while the arachnoid mater and pia mater are referred to as leptomeninges (smooth membrane).
Etiology
The most common cause of SAH is aneurysm rupture (85%). This was followed by nonaneurysmal perimesencephalic hemorrhage in 10% and the remaining 6% due to other conditions.
Epidemiology
The incidence of acute subarachnoid hemorrhage is estimated to be 2-22 cases per 100,000 people per year, and 60% of all acute subarachnoid hemorrhages occur in people aged 40 to 60 years.
Based on data from the Indonesian stroke registry in 2012 to 2014, the incidence of subarachnoid hemorrhage was 181 people of 5.411 stroke patients or about 3.3% of the total stroke patients.
There are more women than men, which is about 53.59%.
The estimated 30-day mortality rate is 35%, with high morbidity among survivors
In this case report, a 58-year-old woman is being treated at the Neurology department of dr. Mohammad Hoesin general hospital Palembang due to a sudden decrease of consciousness.
From the anamnesis, it was found that the patient experienced a sudden decrease of consciousness, severe headaches, and projectile vomit (obtained from alloanamnesis), complaints were also accompanied by weakness on both sides of the body, and asymmetrical corners of the mouth. The patient has risk factors: Hypertension since 5 years ago uncontrolled.
From physical examination, sensorium E4M5V4, blood pressure 130/80 mmHg, Heart rate 106 times per minute, respiratory rate 22 times per minute, body temperature 36.8C with a peripheral oxygen saturation of 99%. On neurological examination, the left plicanasolabialis was flat, there was no lateralization but there was an increase in muscle tone and physiological reflexes in all four extremities. Meningeal sign (+): nuchal rigidity, laseque +, kerniq +.
Sirriraj score in this patients is + 2.5
Based on the main complaint, the possibly causes of sudden loss of consciousness are drug poisoning, head trauma and vascular disorders.
we can exclude traumatic brain injury because patient had no history of trauma and on physical examination there were no signs of head trauma. (No hematoma under the skin behind the tympanic membrane or around the orbit. no signs of trauma to the neck)
We can exclude drug poisoning because patient does not have a history of taking drugs that can interfere with consciousness and no signs of poisoning seen on examination of the patient's skin.
So, the most likely diagnosis is due to vascular problems, suspect hemorrhagic stroke (subarachnoid Hemorrhage)
According to AHA/ASA guideline we perform non contrast head ct scan as the gold standard to confirm the diagnosis.
From non contrast CT Scan we got Hyperdense lesions filled the interhemispheric falx, sulci, Sylvian cisterns, suprasellar cisterns, ambient cisterns with widened gyri, suggests a Fisher 3 subarachnoid hemorrhage.
According to AHA/ASA guideline initial severity of SAH should be determined rapidly by use of simple validates scale, using hunt and hess scale and world federation of neurological surgeons. In this pasien we got hunt and hess scale 3 and WFNS grade 3 with mortality rate 19%.
For better control, we decided to treatment the SAH patient in the stroke unit while preparing for DSA and coiling.
AHA/ASA recommend DSA with 3-dimensional rotation angiography for detection of aneurysm in patient with SAH and for planning treatment (to determine whether an aneurysm is amenable to coiling or to expedite microsurgery). AHA/ASA class I level of evidence B (new recommendation)
Patients receive several treatments including:
Head elevation 30 degree
Oxygenation
Sodium chloride 0.9 %
Tranexamic acid
Nimodipine
Paracetamol
And DSA
2 days during treatment the patient suddenly experienced shortness of breath and decreased oxygen saturation with crackles (rhonchi) in both lung fields. There were no changes in consciousness or new neurologic deficits.
the patient was consulted to the anesthesia department for consideration of airway stabilization and intensive care, but the family refused
The patient was also consulted to the internal medicine department and diagnosed as acute pulmonary edema with a differential diagnosis of decompensated HHD. They gave furosemide injection therapy intravenously and digoxin 1x0.125 mg orally and planned for echocardiography during working hours.
This initial management is optimal because according to the guidelines from the ACC/AHA/HRS in 2015, diuretics are recommended in heart failure patients with clinical signs or symptoms of congestion to achieve euvolemic status (dry and warm) with optimal doses.
the patient experienced improvement in shortness of breath and an increase in peripheral oxygen saturation but only lasted a few hours
On the next day, the patient still complained of shortness of breath and from physical examination there were no crackles/ rhonchi, no changes in the level of consciousness or new neurological deficits.
On repeated ECG we found an S wave in lead I, Q wave in lead III and T inversion in lead III. It indicates a change in the position of the heart due to dilatation of the right atrium and ventricle. It can also be found axis deviation to the right.
On echocardiographic examination, LVH preserved EF was found, right ventricular dilatation was accompanied by mild-moderate tricuspid valve regurgitation. The embolism will increase the resistance and pressure in the pulmonary arteries which will then release vasoconstrictor compounds, platelet aggregation, and mast cells. Pulmonary arterial vasoconstriction and hypoxemia will then cause pulmonary arterial hypertension, so that right ventricular pressure increases.
On chest x-ray we found a pulmonary hypertension
From the laboratory result we found increase in plasma levels of D-dimer (in patients with D-dimer 5.51) due to the process of endogenous fibrinolysis which is released in the circulation when a clot is found and hypoxaemia due to shunting and decreased ventilation, a decrease in carbon dioxide (CO2) partial pressure of less than 35 mmHg
Based on the results of anamnesis, physical examination and supporting examinations, the patient was diagnosed with suspect acute pulmonary embolism.
To establish the diagnosis of pulmonary embolism, it is necessary to be supported by anamnesis, physical examination, laboratory examination, and imaging.
Management of pulmonary embolism is respiratory and hemodynamic stabilization, thrombolysis, embolectomy, anticoagulation.
Research has proven that thrombolytic therapy can open thromboembolic plugs and have a positive effect on hemodynamic parameters.
Primary reperfusion is recommended, especially in high-risk pulmonary embolism with systemic thrombolysis. The benefit is greatest when therapy is started within 48 hours of symptom onset, but thrombolysis may still be beneficial in patients with symptom onset 6-14 days.
Systemic thrombolysis has been shown to be effective with satisfactory hemodynamic recovery, but has complications, especially related to intracranial hemorrhage.
In acute high-risk pulmonary embolism the dose of tPA (alteplase) is 100 mg intravenously (IV) given over 2 hours.
This patient has complications of SAH which is a contraindication to systemic thrombolytic therapy. In patients with contraindications to thrombolysis, severe hemodynamic compromise that may lead to death before the effect of tPA is achieved and in patients in whom systemic thrombolysis fails to improve hemodynamic status, surgical embolectomy or CDT should be considered if available.
There is a study from Wei-Chieh Lee et al. in 2018 that the combined administration of intravenous unfractionated heparin (UFH) and non-vitamin K oral anticoagulant (NOAC) could be considered as treatment in life-threatening pulmonary embolism accompanied by intracranial hemorrhage. The use of systemic thrombolysis cannot be given because of intracranial bleeding, UFH was chosen because we can still control the therapeutic dose and can still convert the anticoagulant effect if massive bleeding occurs
But giving Anticoagulation after a history of hemorrhagic stroke poses a therapeutic dilemma.
Fong et al. demonstrated in a recent study that increased intracerebral hemorrhage mortality was associated with patients taking warfarin for atrial fibrillation, The risk of recurrence of intracerebral hemorrhage is generally about 2% to 4% per patient/year, whereas the risk of severe bleeding on warfarin therapy is about 2% to 3% per year and may be higher in the first month.
American Heart Association recommends four weeks after intracerebral hemorrhage to initiate or continue anticoagulation, a meta-analysis by Zhou et al. explained that there is still no definite timetable for when to resume therapy and that further studies are needed
The cause of death in this patient was initially due to right ventricular failure due to pulmonary artery obstruction, where right ventricular dilatation and dysfunction would cause intraventricular septal compression to the left side and tricuspid valve regurgitation.
This can interfere with the filling process of the ventricles. With reduced left ventricular filling, systemic cardiac output will decrease and reduce coronary perfusion. Myocardial infarction occurs as a result of decreased coronary flow which can lead to cardiogenic shock
Cardiogenic shock is a life-threatening condition with a high mortality rate of 40%-60%.
circulatory failure and death
