58
It is not simply bleeding in the brain Usama Ragab Yousif (Msc.) Internal Medicine Department

Intracerebral Hemorrhage Case presentation

Embed Size (px)

Citation preview

Page 1: Intracerebral Hemorrhage Case presentation

It is not simply bleeding in the brain

Usama Ragab Yousif (Msc.)Internal Medicine Department

Page 2: Intracerebral Hemorrhage Case presentation

Case Presentation

Page 3: Intracerebral Hemorrhage Case presentation

Personal History

• 65-year old male, M.I.K., from Bordain, married and have 6 offspring, the youngest is 28 years old, retired (was a driver), cigarette smoker, right handed.

Page 4: Intracerebral Hemorrhage Case presentation

Chief Complaint

• Disturbed conscious level, with right side weakness 5 days before admission.

• The patient was brought comatose to ER.

Page 5: Intracerebral Hemorrhage Case presentation

History of present illness

• According to the statement of the relative who brought the patient, that he was reasonably well 6 days before. Suddenly the night before admission, while eating dinner, he felt weakness of the right side of the body, followed by sudden collapse.

• Since then, he is comatose in ICU.

Page 6: Intracerebral Hemorrhage Case presentation

History of present illness

• There is no history of fever, convulsion, trauma to the head.

• No symptoms suggest other system affection.

Page 7: Intracerebral Hemorrhage Case presentation

History of Past illness

• He is hypertensive and diabetic on no treatment.

• There is no history of any cardiac abnormality.

• Chronic kidney disease on conservative measures.

Page 8: Intracerebral Hemorrhage Case presentation

Family History

• Irrelevant

Page 9: Intracerebral Hemorrhage Case presentation

Examination

Patient is comatose, GCS• Eye movement: Eye to pain→ 2• Speech: no speech → 1• Motor response: flexion to pain → 3

Vital Signs:oBlood Pressure: on admision 200/110oPulse: 110, regular, equal on both sided, of

average volumeoTemperature: 37.8ᵒ

c oRespiratory rate: 25/min

HEENT: normal

Page 10: Intracerebral Hemorrhage Case presentation

Examination (cont.)

Extremities:• Upper limbs: no clubbing, no pigmentations, no pallor, normal muscles and nerves.

• Lower limbs: no edema, no pigmentation.

Back: no pigmentation, no swelling, no spine deformities.

Page 11: Intracerebral Hemorrhage Case presentation

Examination (cont.)

Neurologic examination:oLevel of responsiveness: obtunded; arousable

only with repeated and painful stim; verbal output isunintelligible or nil; some purposeful movement to noxious stimuli.

oPupillary responses: RRRoEye movementsoFundoscopic examinationoCorneal reflex: intact.

Page 12: Intracerebral Hemorrhage Case presentation

Examination (cont.)

Neurologic examination (cont.):oMotor examination:

• Muscle tone: hypotonia in 4 limbs equally distributed.

• Reflexes: hyporeflexia in 4 limbs equally distributed.

oMeningeal signs: no meningeal irritation signs.

oResponse to stimuli: flexion attitude.

Page 13: Intracerebral Hemorrhage Case presentation

Examination (cont.)

Cardiac examination: Normal

Chest examination: there is decrease air entry bilaterally, harsh vesicular breathing, coarse crackles, expiratory rhonci allover the chest.

Abdomen: Normal.

Page 14: Intracerebral Hemorrhage Case presentation

Salient Features

Male, 65 years, smoker, Diabetic, hypertensive and CKD.presented with sudden weakness of the right side of the body and DCL.He is now comatoseHe is hypertensive and diabetic on no treatment. There is no history of any cardiac abnormality.He is a smoker for the last 40 years, used to take 30 cigarette/day. There is no family history of similar illness.

Page 15: Intracerebral Hemorrhage Case presentation

InvestigationsControl Patient

4-11 9.7 WBCs11.5 – 15.5 10.4 (NC/NC) HB150-450 231 Platelets

1.2 INR0.5 – 1.2mg/dL 2.34 Creatinine6 – 20 mg/dL 54 BUN3.5 – 5.5 mmol/L 4.4 K

3.4/7.2 Albumin/TPUp to 33 U/L 19/34 ALT/ASTUp to 1.1 mg/dL 0.39 Bilirubin

199 Blood Glucose

Page 16: Intracerebral Hemorrhage Case presentation

Investigations (con.)

Patient7.46 PH30.4 PCO219.5 HCO388.5% SO24.4 K150 Na

Page 17: Intracerebral Hemorrhage Case presentation

Investigations (cont.)

Page 18: Intracerebral Hemorrhage Case presentation

Investigations (cont.)

Page 19: Intracerebral Hemorrhage Case presentation

Investigations (cont.)

Page 20: Intracerebral Hemorrhage Case presentation

Investigations (cont.)

Pelviabdominal US:- Chronic parencymatous liver disease.- Average sized spleen.- Rt kidney : mild back pressure, no increased in

echogenicity or loss of CMD.- Lt Kidney: sonofree.- Otherwise normal sonographic study.

Page 21: Intracerebral Hemorrhage Case presentation

Management

Page 22: Intracerebral Hemorrhage Case presentation

Epidemiology

• Globally, about 17 million strokes occur every year and stroke is the second leading cause of death after coronary heart disease, and the third most common cause of disability.

1- Krishnamurthi RV: Lancet Glob Health. 2013;1(5):e259.Figure: http://www.who.int/mediacentre/factsheets/fs310/en/

Page 23: Intracerebral Hemorrhage Case presentation

Epidemiology• Globally, the incidence of stroke due to ischemia is 68 %,

while the incidence of hemorrhagic stroke (intracerebral hemorrhage and subarachnoid hemorrhage combined) is 32 %.

• Men have a higher incidence of stroke than women at younger but not older ages, with the incidence reversed and higher for women by age 75 years and older.

Mikulik R: J Intern Med 2015; 278: 145–165.Lozano R, et al: Lancet. 2012 Dec;380(9859):2095-128.

Page 24: Intracerebral Hemorrhage Case presentation

In brief stroke is either:

Page 25: Intracerebral Hemorrhage Case presentation

Presentation• Sudden onset• Focal neurological deficit• Progresses over minutes to hours• Depends on location• Symptoms include:

SUDDEN numbness or weakness of face, arm or leg SUDDEN confusion, trouble speaking or understanding. SUDDEN trouble with vison. SUDDEN trouble walking, dizziness, loss of balance or coordination. SUDDEN severe headache.

Page 26: Intracerebral Hemorrhage Case presentation

Review of Anatomy• Blood reaches the brain through 2 systems:1. The carotid system (Anterior Circulation)2. The vertebral system (Posterior Circulation)

Page 27: Intracerebral Hemorrhage Case presentation

Stroke. 2015;46:2032-2060.

Page 28: Intracerebral Hemorrhage Case presentation

Emergency Diagnosis and Assessment

1. A baseline severity score should be performed as part of the initial evaluation of patients with ICH (Class I; Level of Evidence B).

2. Rapid neuroimaging with CT or MRI is recommended to distinguish ischemic stroke from ICH (Class I; Level of Evidence A).

3. CTA and contrast-enhanced CT may be considered to help identify patients at risk for hematoma expansion (Class IIb; Level of Evidence B), and CTA, CT venography, contrast-enhanced CT, contrastenhanced MRI, magnetic resonance angiography and magnetic resonance venography, can be useful to evaluate for underlying structural lesions including vascular malformations and tumors when there is clinical or radiological suspicion (Class IIa; Level of Evidence B).

Page 29: Intracerebral Hemorrhage Case presentation

• Maximum score described is 5 in which % of mortality at 30 days is nearly 100%.

• Although an ICH Score of 6 is possible with the scale, this is rarely observed and is considered highly likely to be fatal.

ICH Score

JC Hemphill et al: Stroke 32:891, 2001; JC Hemphill et al: Neurology 73:1088,2009.

Page 30: Intracerebral Hemorrhage Case presentation

Neuroimaging CT is very sensitive for identifying acute hemorrhage and is considered the

“gold standard”;

Gradient echo and T2* susceptibility-weighted MRI are as sensitive as CT for detection of acute hemorrhage and are more sensitive for identification of prior hemorrhage.

CT angiography (CTA) and contrast-enhanced CT may identify patients at high risk of ICH expansion based on the presence of contrast within the hematoma, often termed a spot sign. A larger number of contrast spots suggests even higher risk of expansion.

MRI, magnetic resonance angiography, magnetic resonance venography, and CTA or CT venography can identify specific causes of hemorrhage, including arteriovenous malformations, tumors, moyamoya, and cerebral vein thrombosis.

Cerebrovasc Dis. 2013;35:582–589.

Page 31: Intracerebral Hemorrhage Case presentation

CT scans (without contrast enhancements):sensitivity= 89%specificity= 100% MRI scan:sensitivity= 83%specificity= 98%

CT imaging is also sensitive for detecting SAH (although by itself does not rule it out), and CTA can readily identify intracranial aneurysms.

On CT brain, hemorrhage appears as hyperdense region, i.e. more white

Case courtesy of A.Prof Frank Gaillard, Radiopaedia.org, rID: 10598

Page 32: Intracerebral Hemorrhage Case presentation

Investigations (cont.)

Page 33: Intracerebral Hemorrhage Case presentation

The CT angiographic (CTA) spot sign is defined as unifocal or multifocal contrast enhancement within an acute primary intracerebral haemorrhage (ICH) visible on CTA source images and discontinuous from adjacent normal or abnormal blood vessels . It should not be present on pre-contrast images. It corresponds to a site of active, dynamic haemorrhage and is an independent predictor of ICH growth and poor outcome

The CT angiographic (CTA) spot sign

Lancet Neurol. 2012;11 (4): 307-14.

Page 34: Intracerebral Hemorrhage Case presentation

LocalizationCerebellar Pontine Basal ganglia

10% 10% 80%

Page 35: Intracerebral Hemorrhage Case presentation

Remember

Page 36: Intracerebral Hemorrhage Case presentation

Remember

Page 37: Intracerebral Hemorrhage Case presentation

Investigations (cont.)

Page 38: Intracerebral Hemorrhage Case presentation

Investigations (cont.)Modified Fisher scale on CT brain (predict risk of vasospasm):

Risk of vasospasm IVH SAH24% - No or minimal Grade I33% + Minimal Grade II33% - Diffuse focal or thick Grade III40% + Diffuse focal or thick Grade IV

Frontera, Jennifer A., et al. "Prediction of Symptomatic Vasospasmafter Subarachnoid Hemorrhage: the Modified Fisher Scale." Neurosurgery 59.1 (2006): 21-27.

Page 39: Intracerebral Hemorrhage Case presentation

Fisher, CM, Kistler, JP, Davis, JM. Relation of cerebral vasospasm to subarachnoid hemorrhage visualized by CT scanning. Neurosurgery 1980; 6:1.Frontera, Jennifer A., et al. "Prediction of Symptomatic Vasospasmafter Subarachnoid Hemorrhage: the Modified Fisher Scale." Neurosurgery 59.1 (2006): 21-27.

Page 40: Intracerebral Hemorrhage Case presentation

Ageing blood on MRIThe imaging characteristics of blood on MRI are variable and change with the age of the blood.In general, five stages of haematoma evolution are recognised:

isointense on T1isointense to hyperintense on T2

1- Hyperacute

T2 signal intensity drops (T2 shortening)T1 remains intermediate-to-long

2- Acute (1-2 days)

T1 signal gradually increases (T1 shortening) to become hyperintense

3- Early subacute (2-7days)

increase in T2 signal  4- Late subacute (7-14days)low on both T1 and T2 5- Chronic (>14-28 days)

Page 41: Intracerebral Hemorrhage Case presentation

Exapmple to Subacute ICH in MRI

Page 42: Intracerebral Hemorrhage Case presentation

Hemostasis and Coagulopathy, Antiplatelet Agents,and DVT Prophylaxis

1. Patients with a severe coagulation factor deficiency or severe thrombocytopenia should receive appropriate factor replacement therapy or platelets, respectively (Class I; Level of Evidence C).

2. Patients with ICH whose INR is elevated because of VKA should have their VKA withheld, receive therapy to replace vitamin K–dependent factors and correct the INR, and receive intravenous vitamin K (Class I; Level of Evidence C). PCCs may have fewer complications and correct the INR more rapidly than FFP and might be considered over FFP (Class IIb; Level of Evidence B). rFVIIa does not replace all clotting factors, and although the INR may be lowered, clotting may not be restored in vivo; therefore, rFVIIa is not recommended for VKA reversal in ICH (Class III; Level of Evidence C).

Page 43: Intracerebral Hemorrhage Case presentation

Hemostasis and Coagulopathy, Antiplatelet Agents,and DVT Prophylaxis

3. For patients with ICH who are taking dabigatran, rivaroxaban, or apixaban, treatment with FEIBA (factor eight inhibitor bypassing activity), other PCCs, or rFVIIa might be considered on anindividual basis. Activated charcoal might be used if the most recent dose of dabigatran, apixaban, or rivaroxaban was taken <2 hours earlier. Hemodialysis might be considered for dabigatran (Class IIb; Level of Evidence C).

4. Protamine sulfate may be considered to reverse heparin in patients with acute ICH (Class IIb; Level of Evidence C).

5. The usefulness of platelet transfusions in ICH patients with a history of antiplatelet use is uncertain (Class IIb; Level of Evidence C).

6. Although rFVIIa can limit the extent of hematoma expansion in noncoagulopathic ICH patients, there is an increase in thromboembolic risk with rFVIIa and no clear clinical benefit in unselected patients. Thus, rFVIIa is not recommended (Class III; Level of Evidence A). It was also not recommended by ESO, 2010

Stroke. 2015; 46: 3020-3035 International journal of stroke 9.7 (2014): 840-855.

Page 44: Intracerebral Hemorrhage Case presentation

Hemostasis and Coagulopathy, Antiplatelet Agents,and DVT Prophylaxis

7. Patients with ICH should have intermittent pneumatic compression for prevention of venous thromboembolism beginning the day of hospital admission (Class I; Level of Evidence A). Graduated compression stockings are not beneficial to reduce DVT or improve outcome (Class III; Level of Evidence A).

8. After documentation of cessation of bleeding, low dose subcutaneous low-molecular-weight heparin or unfractionated heparin may be considered for prevention of venous thromboembolism in patients with lack of mobility after 1 to 4 days from onset (Class IIb; Level of Evidence B).

9. Systemic anticoagulation or IVC filter placement is probably indicated in ICH patients with symptomatic DVT or PE (Class IIa; Level of Evidence C).

The decision between these 2 options should take into account several factors, including time from hemorrhage onset, hematoma stability, cause of hemorrhage, and overall patient condition (Class IIa; Level of Evidence C).

Page 45: Intracerebral Hemorrhage Case presentation

Hemostasis and Coagulopathy, Antiplatelet Agents,and DVT Prophylaxis

Page 46: Intracerebral Hemorrhage Case presentation

Hypertension in acute stroke a management dilemma

Hemorrhagic strokeThe conflict1:

(1) Severe elevations in BP may worsen ICH.(2) Enlargement of the hematoma is associated with neurologic deterioration and worse outcomes. These observations indicate that significant improvements in patient outcome from ICH can be achieved by minimizing hematoma enlargement.

1- Stroke 2007; 38:1072–1075.

Cerebral Infarction

In patients with markedly elevated blood

pressure who do not receive fibrinolysis, a

reasonable goal is to lower blood pressure

by 15% during the first 24 hours after

onset of stroke. The level of blood

pressure that would mandate such

treatment is not known, but consensus

exists that medications should be withheld

unless the systolic blood pressure is >220

mm Hg or the diastolic blood pressure is

>120 mmHg. (Class I; Level of Evidence C)

Page 47: Intracerebral Hemorrhage Case presentation

Hypertension in acute stroke a management dilemma (cont.)

The guidelines:For ICH patients presenting with SBP between 150 and 220 mm Hg and without

contraindication to acute BP treatment, acute lowering of SBP to 140 mm Hg is safe (Class I; Level of Evidence A) and can be effective for improving functional outcome (Class IIa; Level of Evidence B).

For ICH patients presenting with SBP >220 mmHg, it may be reasonable to consider aggressive reduction of BP with a continuous intravenous infusion and frequent BP monitoring (Class IIb; Level of Evidence C).

This is also supported by European Stroke Organisation (ESO) guidelines in 2014 who recommends In acute ICH within 6 h of onset, intensive blood pressure reduction (systolic target <140 mmHg in <1 h) is safe and may be superior to a systolic target <180 mmHg. No specific agent can be recommended.

Stroke. 2015; 46: 3020-3035 International journal of stroke 9.7 (2014): 840-855.

Page 48: Intracerebral Hemorrhage Case presentation

Hypertension in acute stroke a management dilemma (cont.)

Studies have been carried out in that respect:(1)In a randomized controlled trial [INTensive Blood Pressure Reduction in

Acute Cerebral Hemorrhage trial (INTERACT1)]1 on 404 patients with acute spontaneous ICH, intensive BP lowering treatment (target SBP 140 mmHg), compared with traditional management (target SBP 180 mmHg), was associated with a reduction in hematoma growth at 24 h (14 vs. 26%; p = 0.04).

(2) Most recently, the main phase [(INTERACT2)]2 trial has shown no increase in death or serious adverse events from early intensive BP lowering in eligible patients with elevated SBP.

1- Stroke. 2012;43:2236–2238. AND Lancet Neurol. 2008 May;7(5):391-9. 2- N Engl J Med. 2013;368:2355–2365.

Page 49: Intracerebral Hemorrhage Case presentation

Hypertension in acute stroke a management dilemma (cont.)

Studies have been carried out in that respect:

(3) Antihypertensive Treatment of Acute Cerebral Hemorrhage II (ATACH-2) trial, involved 1000 patient, 500 were assigned to intensive treatment and 500 to standard treatment.

• mean systolic blood pressure of 200.6 mmHg at baseline.• Results showed that; the treatment of participants with intracerebral

hemorrhage to achieve a target systolic blood pressure of 110 to 139 mmHg did not result in a lower rate of death or disability than standard reduction to a target of 140 to 179 mm Hg.

3- N Engl J Med 2016; 375:1033-1043

Page 50: Intracerebral Hemorrhage Case presentation

Treatment (cont.)Factors Recommendation

General Monitoring and Nursing

Initial monitoring and management of ICH patients should take place in an intensive care unit or dedicated stroke unit with physician and nursing neuroscience acute care expertise (Class I; Level of Evidence B).

Airway &Breathing

Supplemental oxygen should be provided to maintainoxygen saturation >94% (Class I; Level of Evidence C).Supplemental oxygen is not recommended in nonhypoxic patients with acute ischemic stroke (Class III; Level of Evidence B).

Mobilization Early mobilization of less severely affected patients and measures to prevent subacute complications of stroke are recommended (Class I; Level of Evidence C).

Nutrition A formal screening procedure for dysphagia should be performed in all patients before the initiation of oral intake to reduce the risk of pneumonia (Class I; Level of Evidence B).Insert a nasogastric tube if the patient fails the swallow test.Consider PEG only if prolonged enteral feeding is required (Class I; Level of Evidence B).

Stroke. 2015; 46: 3020-3035

Page 51: Intracerebral Hemorrhage Case presentation

Infection and fever

Treatment of fever after ICH may be reasonable (Class IIb; Level of Evidence C).Sources of hyperthermia (temperature >38°C) should be identified and treated, and antipyretic medications should be administered to lower temperature in hyperthermic patients with stroke (Class I; Level of Evidence C).Routine use of prophylactic antibiotics has not been shown to be beneficial (Class III; Level of Evidence B).Patients with suspected pneumonia or urinary tract infections should be treated with appropriate antibiotics (Class I; Level of Evidence A).

Seizures Clinical as well as EEG documented seizures should be treated with antiseizure drugs (Class I; Level of Evidence A).

Prophylactic antiseizure medication is not recommended (Class III; Level of Evidence B).

Blood Glucose

Glucose should be monitored. Both hyperglycemia and hypoglycemia should be avoided (Class I; Level of Evidence C).

Treatment (cont.)

Page 52: Intracerebral Hemorrhage Case presentation

Prolonged recumbency

As regard ICH, After documentation of cessation of bleeding, lowdose subcutaneous low-molecular-weight heparin or unfractionated heparin may be considered for prevention of venous thromboembolism in patients with lack of mobility after 1 to 4 days from onset (Class IIb; Level of Evidence B).Patients with ICH should have intermittent pneumatic compression for prevention of venous thromboembolism beginning the day of hospital admission (Class I; Level of Evidence A).

Brain dehydratin measures

Corticosteroids should not be administered for treatment of elevated ICP in ICH (Class III; Level of Evidence B). In agreement with International stroke foundation guidelines, 2010 (A)

Treatment (cont.)

National Stroke Foundation – Australia (2010)

Page 53: Intracerebral Hemorrhage Case presentation

Prevention of Recurrent ICH1. BP should be controlled in all ICH patients (Class I; Level of Evidence

A). Measures to control BP should begin immediately after ICH onset (Class I; Level of Evidence A). A long-term goal of BP <130 mmHg systolic and 80 mmHg diastolic is reasonable (Class IIa; Level of Evidence B).

2. Lifestyle modifications, including avoidance of alcohol use greater than 2 drinks per day, tobacco use, and illicit drug use, as well as treatment of obstructive sleep apnea, are probably beneficial (Class IIa; Level of Evidence B).

3. Avoidance of long-term anticoagulation with warfarin as a treatment for nonvalvular atrial fibrillation is probably recommended after warfarin-associated spontaneous lobar ICH because of the relatively high risk of recurrence (Class IIa; Level of Evidence B).

Page 54: Intracerebral Hemorrhage Case presentation

Prevention of Recurrent ICH4. The optimal timing to resume oral anticoagulation after anticoagulant-

related ICH is uncertain. Avoidance of oral anticoagulation for at least 4weeks, in patients without mechanical heart valves, might decrease the risk of ICH recurrence (Class IIb; Level of Evidence B). If indicated, aspirin monotherapy can probably be restarted in the days after ICH, although the optimal timing is uncertain (Class IIa; Level of Evidence B).

5. The usefulness of dabigatran, rivaroxaban, or apixaban in patients with atrial fibrillation and past ICH to decrease the risk of recurrence is uncertain (Class IIb; Level of Evidence C).

6. There are insufficient data to recommend restrictions on the use of statins in ICH patients (Class IIb; Level of Evidence C).

Page 55: Intracerebral Hemorrhage Case presentation

Statins and ICHThere are conflicting reports regarding the use of statins in patients with ICH.

Stroke Prevention With Aggressive Reduction in Cholesterol Levels (SPARCL)study, the benefit of high-dose atorvastatin in reducing recurrent ischemic stroke was offset in part by an increased risk of ICH. However it was non significant.

Also a study in 2012 over 163 patients with ICH 40 was on statin treatment, published in Stroke journal concluded that Statin use in patients with ICH is independently associated with microbleeds

However another metanalysis in 2013, studied 31 randomized controlled trials that included 91 588 statin-treated patients found no significant association between statin use and ICH (OR, 1.08; 95% CI, 0.88–1.32; P=0.47).

It remains unclear whether statins should be continued or discontinued in ICH patients.

Stroke. 2012;43:2677-2681Neurology. 2008;70(24 Pt 2):2364–2370.Stroke.2012;43:2149–2156.

Page 56: Intracerebral Hemorrhage Case presentation

By the year 2000 the commonest killers such as coronary heart disease, stroke, respiratory, diseases and many cancers will be wiped out.

AnonymousIrish Times (24 Apr 1987)

I think this was a joke

Page 57: Intracerebral Hemorrhage Case presentation

Don’t forget rehabilitation

Page 58: Intracerebral Hemorrhage Case presentation

ThanksTIME =

LIFE