HEMATOLOGY 6/30 7/1 7/2 7/3 7/4

WBC: increased Morotti A (1) increased

• Leukocytes interact with platelets, endothelium and coagulation factors, and have
been widely recognized as important contributors to facilitating hemostasis in -same reason (most probably because of the
physiologic and pathologic conditions. rebleeding)
• Acute leukocytosis shifts the hemostatic balance in favor of coagulation and
may therefore play an important role in the arrest of bleeding after an ICH occurs.

• Higher WBC counts accompany more severe ICH as measured by reduced

consciousness, higher baseline hematoma volume and intraventricular
hemorrhage (IVH) presence.
• Leukocyte count has also been associated with higher risk of early neurological
deterioration, increased long term mortality and poor functional outcome
• Leukocytosis does not independently predict poor ICH prognosis when controlling
for other outcome determinants including age, baseline hematoma volume and
admission Glasgow Coma Scale

RBC: decreased decreased

Hgb: increased Zheng H (2) increased

• RBCs lysis occurs within 24 h of ICH and induces the release of Hb and heme,
which are taken up by microglia and neurons; heme can be degraded by HO into -same reason (most probably because of the
biliverdin, carbon monoxide and iron. rebleeding)
• All of Hb, heme and iron causes significant brain edema after the first 24 h, which
is related to a threefold increase of BBB permeability

Hct: decreased Hemorrhage decreased

-the plasma volume has compensated for fluid loss while the red blood cells that -same reason (most probably because of the
have been lost cannot be replaced for days rebleeding)

MCV: increased

-due to rbc lysis

MCHC: increased decreased

-due to rbc lysis -due to rbc lysis

RDW: increased increased

-due to rbc lysis -due to rbc lysis

Neutrophil: increased Zheng H (2) increased
Neutrophils or polymorphonuclear leukocytes (PMNs) are the first leukocytes to
infiltrate the nervous system within 4-5 h after ICH, and reach a peak value at 3 days -same reason (most probably because of the
rebleeding)
Morotti A
• Neutrophils are the first inflammatory cells to invade the central nervous
system when an ICH occurs.
• neutrophils exhibit significant pro-coagulant properties:

1. neutrophils shift the coagulation balance in favor of thrombus formation

through significant expression and release of tissue factor (TF) (24).
2. neutrophils indirectly increase the amount of active TF downregulating the TF
pathway inhibitor
3. Neutrophil extracellular traps can activate platelets, factor X and factor XII,
enhance thrombin generation and contribute to stabilization of the fibrin clot as
well

• Neutrophils’ activation in the hyperacute ICH phase may therefore promote a

procoagulant state that limits hematoma expansion.

lymphocytes: decreased decreased

ESR increased

Zheng H (2)

Sign of acute inflammation

Inflammatory response took place in and around the

hematoma after ICH with the infiltration of
neutrophils and macrophages and activation of
microglia. Inflammation can cause cell swelling and
BBB disruption, and then causes brain edema.
Activated microglia and infiltrating leukocytes release
cytotoxic mediators contributing to secondary injury

Neutrophils or polymorphonuclear leukocytes

(PMNs) are the first leukocytes to infiltrate the
nervous system within 4-5 h after ICH, and reach a
peak value at 3 days

Microglia reaches a peak at 72 h, begin to decrease

by a week and return to basal levels by 21 days after
ICH.

CHEMISTRY

Glucose: increased

BUN: normal increased

Crea: normal or slightly decreased
decreased

16.9 33
INCREASED BUN:Creatinine ratio
Normal
Reason: Cushing’s ulcer?

González-González JA (4)
Higher BUN is associated with upper GI
bleeding

Tomizawa (5)
A BUN/Cre ratio > 30 is a useful metric by which
to diagnose upper GI bleeding

Na+: slightly increased

Albumin: decreased Caironi P. (3)

Hypoalbuminemia:

1. A decrease in its absolute content (decreased in production)

2. Altered water metabolism
3. A redistribution from the intravascular to the interstitial space, due to
increased capillary permeability

1 Morotti A, Phuah CL, Anderson CD, Jessel MJ, Schwab K, Ayres AM, Pezzini A, Padovani A, Gurol ME, Viswanathan A, Greenberg SM. Leukocyte count and intracerebral hemorrhage expansion. Stroke. 2016 Jun;47(6):1473-8.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4879062/

2 Zheng H, Chen C, Zhang J, Hu Z. Mechanism and therapy of brain edema after intracerebral hemorrhage. Cerebrovascular diseases. 2016;42(3-4):155-69.

https://www.karger.com/Article/Abstract/445170

3 Caironi P, Gattinoni L. The clinical use of albumin: the point of view of a specialist in intensive care. Blood Transfusion. 2009 Oct;7(4):259.
https://pubmed.ncbi.nlm.nih.gov/20011637/

4 González-González JA, García-Compean D, Vázquez-Elizondo G, Garza-Galindo A, Jáquez-Quintana JO, Maldonado-Garza H. Nonvariceal upper gastrointestinal bleeding in patients with liver cirrhosis. Clinical features, outcomes and predictors of in-
hospital mortality. A prospective study. Annals of hepatology. 2016 Mar 15;10(3):287-95.
https://pubmed.ncbi.nlm.nih.gov/21677330/

5 Tomizawa M, Shinozaki F, Hasegawa R, Togawa A, Shirai Y, Ichiki N, Motoyoshi Y, Sugiyama T, Yamamoto S, Sueishi M. Reduced hemoglobin and increased C-reactive protein are associated with upper gastrointestinal bleeding. World Journal of
Gastroenterology: WJG. 2014 Feb 7;20(5):1311.

https://www.ncbi.nlm.nih.gov/pmc/articles/pmc3921513/
 Increase in ICP BBB Site Location Mechanism More info Cause

Cytotoxic edema Intact Gray Intracellular Cellular failure The glucose supply for brain cells is remarkably diminished by • Hypoxic ischemic brain injury (near
deterioration of the brain blood flow after cerebral ischemia > drowning, cardiac arrest)
decrease of intracellular ATP production > failure of intra- • Traumatic brain injury
extracellular Na+ transport systems and excessive intracellular • Metabolic disease (urea cycle
Na+ accumulation > abnormal entry of extracellular fluid into disorders, organic acidemias)
cells, resulting in cell swelling > outflow of Na+ from blood • Hepatic encephalopathy associated
vessels is accelerated as the body tries to improve decreases with fulminant hepatic failure
of extracellular Na+ and fluid > induces an extravasation of • Reye’s syndrome
fluid without BBB disruption, and causes extracellular fluid • Infections (encephalitis, meningitis)
accumulation > increase of brain volume > and ICP. • Diabetic ketoacidosis
• Toxic ingestions (aspirin, ethylene
glycol, methanol, endosulfan, ecstasy)
• Water intoxication/ hyponatremia
Vasogenic edema Disrupted White Extracellular Increase vascular endothelial tight junctions are disrupted by inflammatory • Brain tumors
permeability reactions and oxidative stress activated glial cells release • Brain abscess
vascular permeability factors and inflammatory factors, and • Stroke
these factors accelerate blood-brain barrier (BBB) • Hypercapnia
hyperpermeability > extravasation of fluid and albumin > • Posterior reversible encephalopathy
extracellular accumulation of fluid into the cerebral syndrome associated with hypertension
parenchyma > extravasated fluid accumulates outside the • Hepatic encephalopathy associated with
cells, > excessive extracellular accumulation of fluid > fulminant hepatic failure
Increase of brain volume > Increase in ICP • Metabolic disease (urea cycle disorders,
organic acidemias)
• Diabetic ketoacidosis
• Lead toxicity
• High altitude cerebral edema
Interstital edema Intact White Extracellular Impaired CSF Obstruction of flow through ventricular system pathway Obstructive hydrocephalus
outflow (monroe, aqueduct of sylviuys or 4th ventricular outlet) >
Excessive accumulation of CSF > Increase ICP
HYPERTENSION - THE DATA IS INSUFFICIENT TO CONCLUDE THIS

There was no mention in the history

the data is insufficient since the BP upon admission was not recorded

No data on the subsquent measuring of the BP

WHAT IS THE LEAST BP THAT CAN CAUSE BLEED


Data:

most common cause of ICH (35%)

Cigarette (80% increased risk of ICH)

Uncontrolled DM (5% )

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MOYA MOYA

CEREBRAL ATROPHY on CT SCAN

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AVM

annual bleeding risk of 2 % to 4%

most common in young adults (20–40 years of age, most commonly at about 30 years old)

common clinical manifestation of AVMs is seizure (20%–45%)

Temporal lobe (16%)

*remove “more common in male” cause no gender predilection based on the most recent study*

add most common location

avm = headache and seizures

dx= ct angiogtram (vontrast iv then ct scan) or 4 vessel angiogram/DSA (put catheter from femoral artery to cerebral circulation; visualized 2 ICA and Vertebral artery; you want
to identify the feeding vessels; no capillaries; if what is the venous drainage and arterial feeder for treatment planning; spetzler-martin = scoring system for critical location = if
where is the eloquent area; risky ba)

WHEN TO SUSPECT AV MAL? SO LOCATION BEH

how to dx = cannot be ruled out without angiogram

==

CVM - read if to include or not