This document summarizes key points from a review course on critical care medicine given by Dr. Anand Tiwari. It discusses traumatic brain injury epidemiology and mechanisms of injury. It also covers principles of prevention, emergency care, critical care, and brain-specific therapies. Specific topics include intracranial hypertension management, imaging and monitoring, and guidelines for neurosurgical intervention.
17. (a) a lateral view
the base of the occiput to upper border of
first thoracic vertebrae,
(b) an anterior-posterior view
C2 to T1 spinous processes.
(c) an open-mouth odontoid view
C1 lateral masses as well as the whole
odontoid process
anand tiwari reveiw course 2014
21. Mild DAI Moderate DAI Severe DAI
coma between 6
and 24 hours
coma for more
than 24 hours
without
presence of
decerebrate
posturing
coma for more
than 24 hours
and with
presence of
decerebrate
posturing as a
motor response
on nociceptive
stimulation.
anand tiwari reveiw course 2014
23. Definite role in defining shear injuries and
for prediction of prognosis
anand tiwari reveiw course 2014
24. F
A
S
T
H
U
G
anand tiwari reveiw course 2014
Give your patient a fast hug (at least) once a day.
Vincent JL.
25. Crystalloids NS,RL
Colloids
Blood transfusion Trigger
Use of vasopressor- Dopamine/noradrenaline
anand tiwari reveiw course 2014
26. Feeding ASAP ,<24 HRS
Hyper catabolic
NG feed ? Orogastric tube Enteral route
Can consider prokinetic
PEG long term
anand tiwari reveiw course 2014
Perel P, Yanagawa T, Bunn F, Roberts IG, Wentz R. Nutritional support for head-injur
patients. Cochrane Database of Systematic Reviews 2006, Issue 4. Art. No.:
CD001530. DOI: 10.1002/14651858.CD001530.pub2.
Early nutritional therapy in trauma: after A, B, C, D, E, the
importance of the F (FEED)
Alberto Bicudo-Salomão, ACBC-MTI
; Renata Rodrigues de MouraII
;
José Eduardo de Aguilar-Nascimento, TCBC-MTIII
Rev. Col. Bras. Cir. vol.40 no.4 Rio de Janeiro July/Aug. 2013
32. ** Early Rx -- Carbapenem .
**Topical (intrathecal or intraventricular)
therapy colistin (off label ) for A.baumanii
meningitis.
Craniofacial
trauma
CSF leak
new onset
fever
Median time
presentation 12 days.
suspicion of gram
negative meningitis
124 Case Report- A.baumanii meningitis
33. Know your ICU/organism prevalent and
resistant pattern
Preemptive antibiotics ????
Stratify risk factors
Site specific ,bbb penetration
Other factors
anand tiwari reveiw course 2014
34. Which mode?
No permissive hypercapnia
Peep ???
Weaning—
Off ventilator does not mean extubation
anand tiwari reveiw course 2014
Hyperventilation
38. Intracranial pressure monitoring
1.comatose patients with-
Glasgow Coma Scale (GCS) 3-8 with abnormal computed
tomography (CT) scans
2.Normal CT scans with two or more of the following
features at admission:
Age over 40,
Unilateral or bilateral motor posturing, or
A systolic blood pressure of less than 90 mm Hg.
anand tiwari reveiw course 2014
39. anand tiwari reveiw course 2014
] The optic nerve sheath diameter
measurement was found to be well-
correlated with the values of
ICP and its value significantly increased to
7.0 ± 0.58 mm, when ICP rose in value to
>20 mm Hg
40. EEG-SEP monitoring reflects to remaining
metabolic activity of brain parenchyma.
EEG recordings usually get suppressed and
difficult to interpret during deep sedation.
anand tiwari reveiw course 2014
41. Surgical decompression
CSF drainage
Decompressive craniectomy
Osmotherapy
Hyperventilation
Hypotheramia
Barbiturate coma
Steroids
Cerebral vasospasm-nimodipine
Seizure prophylaxis
anand tiwari reveiw course 2014
Fig. 7. The Columbia
stepwise protocol for ICP
46. In this prospective evaluation of early PTS
prophylaxis,
LEV did not outperform PHE.
Cost and need for serum monitoring should
be considered in guiding the choice of
prophylactic agent.
anand tiwari reveiw course 2014
48. An epidural hematoma (EDH) greater than 30
cm3
should be surgically evacuated regardless of
the patient's Glasgow Coma Scale (GCS) score.
An EDH less than 30 cm3
and with less than a 15-
mm thickness and with less than a 5-mm midline
shift (MLS) in patients with a GCS score greater
than 8 without focal deficit can be managed
nonoperatively with serial computed
tomographic (CT) scanning
close neurological observation in a neurosurgical
center.
anand tiwari reveiw course 2014
50. An acute subdural hematoma (SDH) with a thickness greater
than 10 mm or a MLS greater than 5 mm on CT scan should
be surgically evacuated, regardless of the patient's GCS
score.
All patients with acute SDH in coma (GCS score less than 9)
should undergo intracranial pressure (ICP) monitoring.
A comatose patient (GCS score less than 9) with an SDH less
than 10-mm thick and MLS less than 5 mm should undergo
surgical evacuation of the lesion if the GCS score decreased
between the time of injury and hospital admission by 2 or
more points on the GCS and/or the patient presents with
asymmetric or fixed and dilated pupils and/or the ICP
exceeds 20 mm Hg
anand tiwari reveiw course 2014
54. reduces all cause mortality***
May be beneficial in improving neurological
outcomes
if cooling maintained for 48 hrs.
anand tiwari reveiw course 2014
55. anand tiwari reveiw course 2014
EUROTHERM3235
Recruitment
321 patients have now been recruited to
the trial. Thank you for continuing to enrol!
Basilar skull fracture indicated by any of following:
Bleeding from ear or nose
Clear or serosanguineous fluid running from nose or ear
Swelling and/or discoloration behind ear (Battle’s sign)
Swelling and discoloration around both eyes (raccoon eyes)
Battle’s sign can occur from immediately following injury to within 1–2 hours postinjury.
Raccoon eyes are a sign of anterior basilar skull fracture.
Through thin cribriform plate in upper nasal cavity and allow spinal fluid and/or blood to leak out.
Raccoon eyes with or without drainage from nose are an absolute contraindication to inserting a nasogastric tube or nasotracheal intubation.
The optic nerve sheath diameter measurement was found to be well-correlated with the values of ICP and its value significantly increased to 7.0 ± 0.58 mm, when ICP rose in value to &gt;20 mm Hg On the other hand, TCD also measures rise in ICP indirectly. Pulsatility index (difference between systolic and diastolic flow velocity, divided by the mean flow velocity), is found to be correlated with the increase in ICP.[11] It can signify either rise in the ICP or decrease in the cerebral perfusion pressure (CPP).[11] These non-invasive tools may be used when use of invasive monitoring cannot be used or rather contraindicated.[9,10,11] However, both tools need to be validated in randomized controlled trials before they can be recommended for routine use in patients with severe TBI. If the brain is hypoperfused, oxygen extraction will be increased and SjvO2 will be reduced.[12,13] On the other hand, if CBF is adequate for the brain&apos;s metabolic need, then SjvO2 will remain normal. This monitoring should be used in conjunction with moderate to severe hyperventilation therapy for patients with intracranial hypertension.
Temperature management
TBI initiates several metabolic processes that can exacerbate the injury.[36] Hyperthermia is one of the potential factors exaggerating the secondary injury. Hyperthermia may develop due to infections or some neurogenic mechanisms. Recent observational study of 7145 patients has shown that both degree and duration of early post head injury fever are strongly correlated with outcome.[37] It is prudent to keep the patients normothermic and antipyretics as well as surface cooling can be used to attain this.[36,37,38]
On the other hand, there is evidence that hypothermia may limit some of these deleterious metabolic responses and improve the outcome.[39,40] However, the literature suggests that therapeutic hypothermia should be instituted as soon as practical (in the emergency room) and beneficial effect usually seen when it has been continued for at least 72 h.[40] In a RCT (n = 82), role of moderate hypothermia (32-33°C) in closed head injury (GCS 5-7) patients was found to hasten the neurologic recovery and improved the outcome.[41] A Cochrane review in 2009 analyzed 23 trials with a total of 1614 patients and found no evidence supporting the use of hypothermia during the treatment of TBI, but did find a statistically significant increased risk of pneumonia and other potentially harmful side-effects.[42] The important multicenter randomized controlled trial (The Eurotherm 3235 trial) on therapeutic hypothermia (32-35°C) in ICP reduction following TBI has recently been completed; however, its results is still awaiting and could be important to give better insight about this therapy.[4
n HBOT, 100% oxygen at environmental pressures greater than 1 atmosphere absolute is administered for respiration in an airtight vessel. Therefore, there is a substantial increase in partial pressure of oxygen to the tissues that can help to improve the oxygen delivery to the injured brain tissue and also reduces brain edema. This therapy has shown some promising results to decrease the overall mortality in patients with severe TBI; however, there were no substantial improvement found related to neurological outcome of these patients.[50] In addition, the potential side-effects of oxygen toxicity are also concern. Thus, large well-defined controlled trials are needed to prove its effectiveness in patients with TBI. BI generates many pro-inflammatory mediators and leads to secondary brain injury. The main goal of developing future neuroprotective treatments for TBI is to minimize the detrimental and neurotoxic effects of these inflammatory mediators and help in the regeneration and repair after injury.[51,52,53,54] Many agents such as selfotel, pegorgotein (PEG-SOD), magnesium, deltibant and dexanabinol, statins were investigated; however found to be ineffective in clinical trials. The beneficial role of other agents such as progesterone, thyrotropin-releasing hormone and cyclosporine has yet to be tested in large trials. The other potential area of the target is apoptotic pathways. Many agents are being investigated to block the intermediate pathways related to apoptosis. However, the apoptotic changes are also essential for normal functioning of cells; therefore, blocking the pathways by these agents would lead to possible potential complications.[