Indications for Tracheostomy.

Nora H Cheung, and Lena M Napolitano Respir Care

2014;59:895-919

(c) 2012 by Daedalus Enterprises, Inc.

Glasglow outcome scale
1. Death
2. Vegetative state
3. Low severe disability
4. Upper severe disability
5. Low moderate disability
6. Upper moderate disability
7. Low good recovery
8. Upper good recovery
Condition of unawareness with only reflex responses but with
periods of spontaneous eye opening.
Condition of unawareness with only reflex responses but with
periods of spontaneous eye opening.
Patient who is dependent for daily support for mental or
physical disability, usually a combination of both. If the patient
can be left alone for more than 8h at home it is upper level of
SD, if not then it is low level of SD.
Patients have some disability such as aphasia, hemiparesis or
epilepsy and/or deficits of memory or personality but are able
to look after themselves. They are independent at home but
dependent outside. If they are able to return to work even with
special arrangement it is upper level of MD, if not then it is low
level of MD.
Resumption of normal life with the capacity to work even if pre-
injury status has not been achieved. Some patients have minor
neurological or psychological deficits. If these deficits are not
disabling then it is upper level of GR, if disabling then it is lower
level of GR.
 Brain gut interaction

https://www.ncbi.nlm.nih.gov/pmc/articles/P
MC6047317/
DAMPs and cytokines produced in brain
ischemic tissue are released to the circulation
to gain access to immune or lymphoid organs

After stroke, the brain–gut axis is significantly

distressed by injury-induced DAMPs, cytokine
release, the BBB changes, altered microbiota
or dysbiosis, and leaky gut, resulting in
migration of inflammatory and immune cells
from gut to the brain.

The findings by Benakis et al. show that

inhibition of intestinal IL-17 secreting γδ T-
cells by Treg cells may alleviate poststroke https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6329216/
inflammation in mice.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6329216/

Drugs targeting IL-23 include BI-655066,

briakinumab, guselkumab, tildrakizumab, and
ustekinumab
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4799039/

https://www.ncbi.nlm.nih.gov/pmc/articl
es/PMC3728507/
Heart Brain interaction
electrocardiographic abnormalities are found
in 40% to 100% of SAH patients and 5% SAH
patients have serious cardiac arrhythmias.
Lee et al22 found that in spontaneous and
traumatic brain hemorrhage patients, 7.2% (no
history of cardiac disease patients) show acute
cardiac dysfunction and 43% have LV
hypertrophy.
During the first 3 months after acute ischemic
stroke, 19.0% of patients experience at least 1
serious cardiac adverse event; 28.5% have LV
ejection fraction <50%; and 13% to 29% have
systolic dysfunction.
bout 88% of stroke patients who sustain
damage to the insular cortex in the right
cerebral hemisphere develop myocardial injury
in the weeks after ischemic stroke.
Elevation of serum myocardial enzymes is
reported in 11% to 21% of SAH patients and in
1% to 17% of ischemic stroke patients.
The brain–gut axis and gut–heart axis may mediate cardiac damage after stroke. Stroke
increases intestinal barrier permeability, enabling bacterial and endotoxin translocation to
bloodstream inducing inflammatory responses and proinflammatory cytokine production.
Cytokine production can trigger inflammation, fibrosis, and microvascular and myocardial
dysfunction. Trimethylamine-N-oxide (TMAO) is the hepatic oxidation product of the microbial
metabolite trimethylamine (TMA). TMAO promotes the development of hyper-responsive
platelet phenotype and enhances elevating the risk for heart failure and heart attack. CRP
indicates C-reactive protein; IL, interleukin; and TNF, tumor necrosis factor.
A major source of microvesicles in stroke
Tian et al found that microvesicles were
patients is vascular endothelial cells. Blood-
produced from injured hippocampal cells,
derived microvesicles stimulate release of
transmigrated through the disrupted
endothelial cell cytokine IL-6. IL-6 can induce
endothelial barrier in a platelet-dependent
vascular spasm and lead to coronary
manner, and activated platelets and thereby
syndrome.
induce coagulopathy in TBI model.
endothelial cells secrete microvesicles that can Zhao et al, found that brain-derived
inhibit endothelial NO synthase. Anti– mitochondrial microparticles significantly
endothelial NO synthase activity leads to a increased in the circulation after TBI. The
decline in NO production, causing endothelial mitochondrial microparticles synergized with
dysfunction and impaired vascular relaxation. platelets to facilitate vascular leakage by
the increased endothelial cell microvesicle is disrupting the endothelial barrier. The
related with symptomatic cerebral vasospasm disrupted endothelial barrier allowed the
and predicts infarction post-SAH. release of mitochondrial microparticles into
platelet microvesicles have 50- to 100-fold the systemic circulation to promote
higher specific procoagulant activity than coagulation and enhanced fibrinolysis,
activated platelets and are hence associated vascular fibrin deposition, and thrombosis.
with thrombosis.
Altered platelet activity because of
microvesicles derived from platelets and
injured brain can lead to thromboembolic
events and associated cardiac complications
after brain injury such as stroke or TBI.
Heart Brain interaction