Organic brain syndrome

Source:http://www.nlm.nih.gov/medlineplus/ency/article/001401.htm

Organic brain syndrome (OBS) is a general term used to describe decreased mental function due to a medical disease, other than a psychiatric illness. It is often used synonymously (but incorrectly) with dementia.
Causes

Disorders associated with OBS include:

* Brain injury caused by trauma
o Bleeding into the brain (intracerebral hemorrhage)
o Bleeding into the space around the brain (subarachnoid hemorrhage)
o Blood clot inside the skull causing pressure on brain (subdural hematoma)
o Concussion
* Breathing conditions
o Low oxygen in the body (hypoxia)
o High carbon dioxide levels in the body (hypercapnia)
* Cardiovascular disorders
o Abnormal heart rhythm (arrhythmias)
o Brain injury due to high blood pressure (hypertensive brain injury)
o Dementia due to many strokes (multi-infarct dementia)
o Heart infections (endocarditis, myocarditis)
o Stroke
o Transient ischemic attack (TIA)
* Degenerative disorders
o Alzheimer's disease (also called senile dementia, Alzheimer's type)
o Creutzfeldt-Jacob disease
o Diffuse Lewy Body disease
o Huntington's disease
o Multiple sclerosis
o Normal pressure hydrocephalus
o Parkinson's disease
o Pick's disease
* Dementia due to metabolic causes
* Drug and alcohol-related conditions
o Alcohol withdrawal state
o Intoxication from drug or alcohol use
o Wernicke-Korsakoff syndrome (a long-term effect of excessive alcohol consumption or malnutrition)
o Withdrawal from drugs (especially sedative-hypnotics and corticosteroids)
* Infections
o Any sudden onset (acute) or long-term (chronic) infection
o Blood poisoning (septicemia)
o Brain infection (encephalitis)
o Meningitis (infection of the lining of the brain and spinal cord)
* Other medical disorders
o Cancer
o Kidney disease
o Liver disease
o Thyroid disease (high or low)
o Vitamin deficiency (B1, B12, or folate)

Other conditions that may mimic organic brain syndrome include:

* Depression
* Neurosis
* Psychosis

Symptoms

Symptoms can differ based on the disease. In general, organic brain syndromes cause:

* Agitation
* Confusion
* Long-term loss of brain function (dementia)
* Severe, short-term loss of brain function (delirium)

Exams and Tests

Tests depend on the disorder, but may include:

* Blood tests
* Electroencephalogram (EEG)
* Head CT scan
* Head MRI

Treatment

Treatment depends on the disorder. Many of the disorders are treated mainly with rehabilitation and supportive care to assist the person in areas where brain function is lost.

Medications may be needed to reduce aggressive behaviors that can occur with some of the conditions.
Outlook (Prognosis)

See the specific disorder. Some disorders are short-term and treatable, but many are long-term or get worse over time.

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Splenic injury grading

Source:http://radiopaedia.org/articles/splenic_injury_grading
American Association for the Surgery of Trauma (AAST)

Grade I

* Subcapsular haematoma < 10% of surface area
* Capsular laceration < 1 cm depth

Grade II

* Subcapsular haematoma 10 - 50% of surface area
* Intraparenchymal haematoma < 5 cm in diameter
* Laceration 1 - 3 cm depth not involving trabecular vessels

Grade III

* Subcapsular haematoma > 50% of surface area or expanding
* Intraparenchymal haematoma > 5 cm or expanding
* Laceration > 3 cm depth or involving trabecular vessels
* Ruptured subcapsular or parenchymal haematoma

Grade IV

* Laceration involving segmental or hilar vessels with major devascularization (> 25% of spleen)

Grade V

* Shattered spleen
* Hilar vascular injury with devascularised spleen

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The Rule of SIX in Drug Dosing and Infusion

Source:http://emergencymedic.blogspot.com/2010/08/rule-of-six-in-drug-dosing-and-infusion.html

Supposed as a junior medical officer, you want to start dopamine infusion for a patient in hypovolemic shock (with persistent low BP despite adequate fluid resuscitation). You look up at the drug formulary (just to counter-check) and it states that the dosage for dopamine is "5 mcg/kg/min, increasing gradually using 5-10 mcg/kg/min increments......". Most drug formularies will list dopamine dosages in the form of xxx mcg/kg/min.

So, you decide to start the patient on 10 mcg/kg/min. You remember well what you were taught in med school: dopamine infusion in the range 3 - 5 mcg/kg/min is predominantly for its dopaminergic effect (dopaminergic receptors are present abundantly in the mesenteric vasculature, brain, heart and the kidneys); dosing range from 5 - 10 mcg/kg/min is predominantly for its beta effects and dosage ranges above 10mcg/kg/min up to 20 mcg/kg/min is for its alpha effects.

You inform the staff nurse on duty: "Staff nurse, could you start dopamine infusion for this patient, start with 10 mcg/kg/min, titrating until a desirable blood pressure achieved. Erm.. I think this patient's weight is around 70 kg" Unfortunately, the staff nurse on duty is a junior staff nurse. She looks at you and said "Doctor, can you tell me how do I prepare for the infusion? Each ampoule of dopamine is 200 mg." You look a little bit annoyed, thinking to yourself "you mean you didn't learn that in your nursing school???" Regardless, still the sole responsibility of giving clear, concise and detailed instruction rests on the shoulder of the doctor in charge. You cannot blame the staff nurse of whether she learns that in nursing school or not.

Since you can't get an "answer" from the junior staff nurse, you turn around and ask a senior staff nurse. The senior staff nurse said, "Doctor, I don't know about this 10 mcg/kg/min. But from my experience, if you break open 1 ampoule of dopamine (200 mg) and diluted it into 50 cc, usually most doctors will run the drug at 10 ml/hr.

Huh??? You got more confused!!!

The above scenario is not uncommonly seen. Many nurses, from my experience, either do not understand or have forgotten about the correlation between the xxx mcg/kg/min that is stated in most books and the actual running of how many ml/hr of the diluted dopamine in 100-ml or 50-ml syringe.

The secret of calculating that is by using the RULE of SIX for drug infusion. And I am amazed how many medical students do not know this and how many of them actually do not even know how to derive this formula.

So, in this blog post, I will first prove that this formula is true by deriving it from basic mathematics and then to discuss on the variants of this formula for the ease of practicality.

The Rule of Six for drug infusion states that:

When (6 * body weight of patient) mg of a drug is diluted in 100 ml,

every ml/hr of the drug infused is equal to one mcg/kg/min


In other words,
(6 * BW) mg diluted in 100ml, 1 ml/hr = 1 mcg/kg/min, where BW - body weight

How do we derive that formula? Basic simple algebra......
We break up that equation into two parts:
1 ml/hr ..................... (A)
1 mcg/kg/min ......................(B)

and then we will attempt to prove that (A) = (B)


Now, let's look at the first part of the equation, part (A), namely 1 ml/hr

Let's assume BW = a kg
So,
(6a) mg of Drug A ---- in 100 ml (diluted into 100 ml)

therefore,
1 ml of Drug A = (6a)mg/100

But 1 ml of Drug A is infused over 1 hour (= 60 min)

Therefore, for every min, the amount of drug A infused is:
(6a)mg/(100*60)

But every 1 mg = 1000 mcg.
Therefore, for every min, the amount of drug A infused is:
(6a)*1000 mcg/(100*60)

simplify the equation, for every min, the amount of drug A infused is:
(a) mcg

In other words, part A of the equation (1 ml/hr) can be written as:
(a) mcg...........................(1)


Now, look at part B of the equation, 1 mcg/kg/min

We have assumed that the BW = a kg,

therefore, for every min, the amount of drug A infused is:
(a) mcg............................(2)

Since, (1) = (2), therefore
1 ml/hr = 1 mcg/kg/min if (6*BW) mg of the drug is diluted into 100 ml.

Unfortunately, 100-ml syringes are not easily available in my hospitals. Most of the large syringes are 50-ml syringes.

Nevermind, the rule of 6 can still be applied, but for 50-ml dilution,

(3*body weight) mg of drug A in 50 ml, 1 ml/hr = 1 mcg/kg/min

(this simply because 50 = 100/2, therefore we take 6/2, which is 3 !!).

In other words, the rule of 6 can also be written as:

When (3 * body weight of patient) mg of a drug is diluted in 50 ml,

every ml/hr of the drug infused is equal to one mcg/kg/min



and, by using the same premise,

When (0.3 * body weight of patient) mg of a drug is diluted in 50 ml,

every ml/hr of the drug infused is equal to 0.1 mcg/kg/min



and...


When (0.03 * body weight of patient) mg of a drug is diluted in 50 ml,

every ml/hr of the drug infused is equal to 0.01 mcg/kg/min



Now, let's come back to our case scenario.

Let's apply the rule of 6 in our case. The patient's body weight is 70 kg. Most adults' body weight would be in the range of 60 - 70- kg. Assuming that we are going to dilute into 50 ml, therefore we use the variant:


When (3 * body weight of patient) mg of a drug is diluted in 50 ml,

every ml/hr of the drug infused is equal to one mcg/kg/min


Therefore,
(3*70) mg of dopamine is diluted in 50 ml, every ml/hr is equal to 1 mcg/kg/min.
In other words, 210 mg of dopamine is diluted in 50 ml, 10 mcg/kg/min requires 10 ml/hr.

210 mg ~ approximately 200 mg. Remember that most dopamine ampoules contain 200 mg each.

Therefore, for convenience sake, break open 1 ampoule of dopamine (200 mg), dilute in 50 ml, and just run 10 ml/hr (that will give you 10 mcg/kg/min). No wonder that's what the senior staff nurse said! You see, most drugs are prepared in such a way that it is convenient to use (especially for adult patients) and most people (especially those in places like emergency departments and ICUs), doctors and staff nurses included, are doing it routinely without really understand the principles behind.

In other words, you would not have much problem, if you are infusing drugs such as dopamine, where the drug ampoules are conveniently prepared.

But you will have troubles when it comes to pediatric patients (where the Rule of 6 is particularly useful) and when it comes to infusing other drugs such as adrenaline or noradrenaline (also known as epinephrine and norepinephrine respectively).

Adrenaline infusion, for example, the dosage range is 0.05 mcg/kg/min - 0.2 mcg/kg/min. So how are you going to prepare the dilution and rate of infusion? Bearing in mind too that most adrenaline ampoules come in 1mg/ml packaging. If you apply the rule of 6, then you will have to take your time to break 200 ampoules!! (while the patient is hanging there in a state of shock). Furthermore, since the dosage range is around 0.05 mcg/kg/min, the rate infused per min will be in the decimals - minute amount!

Therefore, we use this variant of the rule:

When (0.03 * body weight of patient) mg of a drug is diluted in 50 ml,

every ml/hr of the drug infused is equal to 0.01 mcg/kg/min


So, for adrenaline, (0.03 * 70) mg of adrenaline diluted in 50 cc, 1 ml/hr = 0.01 mcg/kg/min.

Therefore, for convenience, you just need to break 2 or 3 ampoules (2 - 3 mg) of adrenaline, dilute it to become 50 ml, and infuse at the rate of 5 ml/hr (if you are aiming for 0.05 mcg/kg/min). Bearing in mind too that the rule need not to be applied rigidly, because in the first place, the weight that you estimate is just as it is - an estimation. You can always titrate the infusion rate up and down. But the decimal point and the variant of the rule you are going to use must be decidedly correct because there has been anecdotal report that states that a baby died as a result of "misplaced decimal point (when applying the rule of 6) and the preparation of a dopamine infusion that was 10 times more concentrated than required" (Click on the link to read the article).

I disagree with the writer of that article that the use of the Rule of 6 should be abandoned. The rule of 6 is just a scientific, standalone formula that can be derived objectively from first principles. It is neutral. It is only when we do not understand the principles behind properly, then we will just follow blindly and thus, courting disaster!

Happy infusing!

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Emergency Fluid Therapy

Source:http://www.slideshare.net/drcd2009/emergency-fluid-therapy
Emergency Fluid Therapy - Presentation Transcript

1. Fluid Therapy in Emergency Care Dr. Rashidi Ahmad Medical Lecturer/emergentist School Of Medical Sciences USM Health Campus Kelantan 2 nd Regional Fluid Transfusion Workshop 10 February 2007
2. Outline
* Introduction
* Volume therapy in hemorrhagic shock
o Crystalloid versus colloid
o Hypertonic saline/Small volume resuscitation
o Blood
* Fluid therapy – when? How much?
* Fluid therapy in septic shock
* Endpoint of resuscitation
3. “ The Neglected Disease of Modern Society” Trunkey, DD
4. Trauma Chain of survival Fluid therapy is a part of the factors…
5. Polytrauma?
* A syndrome of combined injuries with ISS > 17 & consequent SIRS for at least 1 day, leading to dysfunction, or failure, of remore organs & vital systems, which themselves had not directly been injured.
Marius Keel et al. Pathophysiology of trauma. Injury (2005) 36, 691-71
6. O2 flux = [ C.O X Hb X SaO2 X k] + [ C.O X PaO2 x 0.003] Principle of fluid therapy in Emergency care
7. Shock
* The viability & normal functioning of multiple organ systems & the whole body depends on continuos adjustment of C.O & DO2 to meet VO2
* C.O   VO2 & DO2 imbalance = cumulative O2 debt
Cumulative O2 debt overwhelms the physiologic reserve of CVS & RS to compensates = SHOCK Mohd Y Rady. Em. Med, 1996
8. Traumatic shock
* Tissue oxygenation is compromised by  DO 2 (hemorrhage) &  VO 2 (inflammatory response).
* Occurs in combination (bleeding, pain, tissue edema, neurogenic shock @ tension pneumothorax).
* Bleeding frequently occurs at multiple sites & is self limiting.
* Penetrating trauma, major bleeds rapidly leads to hypovolemic cardiac arrest
9. Marius Keel, Omar Trentz. Pathophysiology of polytrauma. Injury (2005) 36, 691 - 709
10. Pseudo-shock
11. Fluid Balance Consequences in Early Shock
* Mobilization of ECF
* Haemodilution of plasma
* – ?Coagulation effects
* – Gradual fall in Hb
* Maintenance of vascular space at the expense of the ECF
12. Late shock
* • Capillary leak
* • Loss of plasma volume
* • Tissue edema
* • Organ edema (lung, kidney)
* • Multiple organ failure
13. Phases of Resuscitation in Trauma Care
* Pre-hospital Resuscitation
* ED Resuscitation
* Establishment of Definitive Care
* ICU on going resuscitation
14. Aim of volume resuscitation
* • Early, complete restoration of tissue
* oxygenation
* • Minimal biochemical disturbance
* • Preservation of renal function
* • Avoidance of transfusion complications
15. Goals of Fluid therapy in hemorrhagic shock
* First Priority: Restore volume
* Second Priority: Restore blood - oxygen carrying capacity
* Third Priority: Normalize coagulation status
16. Fluid of choices
* Well-balanced resuscitation fluid resembling ECF
* Rapid volume expansion of IVS
* Sustained expansion
* No sugar
17. Options for fluid resuscitation
* Crystalloid – NS, Lactated Ringers’s solution, hypertonic saline
* Colloid – albumin, gelatine, dextran, starch (VOLUVEN)
* Blood – allogenic blood, autologous blood
* Blood substitutes – cross-linked, polymerize @ conjugated Hb
18. Optimal fluid resuscitation
* No ideal fluid resuscitation
* Combination therapy
* Volume expansion
* O2 carrying capacity of blood, without the need for cross matching @ the risk of transmission
* Restore & maintain the normal composition & distribution of body fluid compartment
19. Crystalloids
* • Ringer’s:
* – Low sodium, lactate load
* • Saline:
* – Hyperchloraemic acidosis, no K+
* • Both:
* – Large volume resuscitation needed (3:1)
20. Crystalloid
21. Crystalloids
* Lower cost
* EC expander
* Greater urinary flow
* Replaces interstitial fluid
* Transient haemodynamic improvement (20 – 30 min)
* Peripheral oedema
* Pulm oedema (protein dilution +  PAOP)
22. Colloids
* Greater cost
* IV expander, do not resuscitate ECF
* Smaller volume (1:1)
* Osmotic diuresis
* Longer duration of persistence (2 – 8 hours)
* Less cerebral oedema
* Coagulopathy
* Pulm oedema (cap. leak state)
*  GFR (hyperoncotic kidney failure syndrome
* Improved rheology
* • Allergic risk (gelatin > dextran > HES)
23. Colloid (no capillary leakage)
24. Colloids versus crystalloids for fluid resuscitation in critically ill patients:
* The Cochrane review: Lancet; Issue 2 Oxford 2000 by Alderson P, Schierhout G, Roberts I, Bunn F
* Conclusion: No evidence that resuscitation with colloids reduces the risk of death compared with crystalloid in patient with traumatic injury
25. The crystalloid–colloid debate has evolved into a colloid-colloid debate
26. Ideal colloid National Research Council – USA (1963)
* Rapidly replaces blood volume losses.
* Restores the haemodynamic balance.
* Normalizes microcirculatory flow.
* Have a sufficiently long intravascular life.
* Be readily metabolized, readily excreted and well tolerated.
* Be free of side effects, especially regarding haemostasis and anaphylactoid reaction
* Be cost effective and contribute to blood savings.
27. Gelatins
* Short acting
* Prevent platelet aggregation induce by ristocetin - minimal effect on coagulation
* May be diuretic
* Allergy risk
* Contain high [Ca 2+ ) ~ facilitate clotting
28.
29. Dextrans
* Good duration of effect
* Good rheological effect (esp Dextran 40)
* Allergy risk
* Significant coagulation effect
* May interfere with cross-match
* Dextran 40 can cause osmotic renal damage
30. Albumin
* Expensive
* • No evidence of benefit
* • Some evidence of harm
* • ANZICS SAFE study:
* – 7000 patients randomized to Alb or NS

31. Starches
* Good duration of effect
* High molecular weight starches impair coagulation
* Medium molecular weight HES has minimal effect
* Possible endothelial benefit
32. Hetastarch (hydroxyethyl starch)
* Derived from corn starch
* Modified natural polymers of amylopectin which breaks down by amylase
*  IV persistence due to substitution of hydroxyethyl group with D – glucose & more of glucose molecules hydroxylated at the C2 position versus the C6 position,
33. Hetastarch evolutionary concept
* A high degree of substitution (> 0.6), a high C2:C6 ratio (> 8), and a high initial MW (> 450 kDa) will maximize the intravascular half-life.
* Polymers with a MW < 50 kDa are eliminated rapidly by glomerular filtration and larger polymers are hydrolysed by amylase into smaller molecules.
34. HAES classification
35. Types of HES
* 1 st HES – marketed in US & Germany, 450kDa, a/w coagulopathy, withdrawn
* Elohes 6% - (200/0.62)
* Lomol 10% - (250/0.45)
* Haes – Steril 6% - (200/0.5)
* Voluven 6% - (130/0.4)
36. Advantages of HES
* Encourages the restoration of cell mediated function and macrophage function after hemorrhagic shock
* Schmand JF et al. Criti Care Med 1995;23:806–14.
* 10% HES (200:0.5) resulted in significantly better systemic haemodynamics and splanchnic perfusion than volume replacement with 20% human albumin
* Boldt J et al. Anesth Analg 1996;83:254–61.
37. HES & allergic reactions Laxenaire MC et al. Anaphylactoid reactions to colloid plasma substitutes: incidence risk factors mechanisms. Annales Francais d’Anesthesie et Reanimation 1994;13:301–10 A French multicenter prospective study.
38. Disadvantages of HES
* Repeated administration of HAES especially high in vivo MW – reduce factor VIII & VWF & renal function (coagulopathy & anuria)
* Haes – Steril solutions, medium MW were widely used for intravascular volume replacement in cardiac surgery.
* Recommended max dose per day: 20 – 33 ml/kg.
39. Voluven
* HES 130/0.4 was developed with the aim of improving the pharmacokinetic & Mw distribution profile of HES 200/0.5
* Their beneficial effects appear to be related more to their action on inflammatory processes than their colloid osmotic power
* It has been shown in few pharmacokinetic studies that voluven solutions were decreased in plasma & tissue storage after repeated administration (50 – 75 ml/kg/d) & less influence on coagulation.
Anest Analg 2003;96:936 – 43 Anesthesiology, V 99, No 1, Jul 2003
40. Hypertonic saline Stackford SR. J Trauma 1998:44:50-8
* High osmolality (2400 mOsmol/L)
* Small Volume Resuscitation
* Reduced cerebral edema
* Reduced trauma-induced immuno-suppression
* CI: dehydration, oliguric renal failure, cardiogenic shock, DKA, coagulopathies or active hemorrhage
* Central pontine myelinosis : NO clinically significant & were not reported
* Practical dose: 200mls 7.5% NaCl in 10 min
41. Hypertonic Saline
42. Velasco IT et al. Hyperosmotic NaCl and severe hemorrhagic shock. Am J Physiol 1980;239:H664-73
* Severely hemorrhaged dogs (40 ml/kg blood loss) re- sponded with a restored arterial pressure and cardiac output following IV bolus injections of 4 mL/kg of 7.5% NaCl,
* A volume equivalent to only 10% of the volume of shed blood
43. Best evidence
* Wade CE et al. Efficacy of hypertonic 7.5% saline and 6% dextran-70 in treating trauma: a meta-analysis of controlled clinical studies. Surgery 1997;122:609-16.
* 14 trials (1200 patients, 8 HSD, 6 HS)
* Conclusion: No differences in survival with HS, HSD, crystalloid
44. Best evidence
* Wade CE et al. Individual patient cohort analysis of the efficacy of hypertonic saline/dextran in patients with traumatic brain injury and hypotension J. Trauma 1997;42:S61-5.
* RCT comparing HSD & HS alone, as compared to crystalloid.
* Conclusion: some benefit of HS in penetrating injuries and those with combined shock and severe head injury.
45. Blood
* Oxygen flux: CO × O 2 content : CO(SaO2 × Hb × 1.34)
* Blood transfusion is reserved for cases of significant or ongoing bleeding.
* Why?
* - Limited blood supply
* - Need to be re warmed
* - Disease transmission
* - Immunosuppressive effect/ risk of infection
* - I ndependent risk factor for post-traumatic organ dysfunction.
46. Blood
* Limit transfusions
* Transfusion threshold < 7g/dl
* Maintenance level 7 – 9 g/dl
* Older patients and those with ischemic heart disease may need higher Hb
47. Alternative choices
* Autologous blood salvage technique
* Blood substitute
* - modified hemoglobins
* - perfluorocarbons
48. Autologous blood salvage technique
* Example: to reinfuse blood loss secondary to a massive hemothorax.
* Tedious & technical, need experienced personal
* Risk of bacterial contamination
* Micro emboli of platelet plugs and fractured red blood cells.
49. Artificial hemoglobin
* Sloan EP et al. Diaspirin cross linked hemoglobin (DCLHb) in the treatment of severe traumatic hemorrhagic shock. a randomized controlled efficacy trial.
* JAMA 1999; 282:1857-1864
* Study terminated prematurely
* Increased number of death in the experimental group.
50. Hemoglobin based oxygen carrier HBOCs
* Analdo BD, Minei JP. Potential of hemoglobin based oxygen carrier in trauma patients.
* Curr Opin Crit Care 2001; 7: 431-436
* Excellent overview relevant to trauma
* Problem: nitric oxide scavenging effects leading to smooth muscle constriction and subsequent blood pressure elevation
51. HBOC- 201
* McNeil JD, Smith Ld, Jenkins DH, et al.
* J Trauma 2001; 50:1063-1075
* Hypotensive resuscitation using a polymerized bovine hemoglobin-based oxygen carrying solution (HBOC- 201) leads to reversal of anaerobic metabolism.
52. Fluid resuscitation: WHEN & HOW MUCH?
* Traditional strategy: to restore patients to a normovolemic state ASAP
* Based on animal studies (1950 – 60) & Vietnam war.
* Recent strategy: judicious use of fluids, SVR
* Lack of randomized controlled studies, lack of implementation
* ? No documentation support the proposed changes actually will improve patient outcome
53.
* Treatment with IV fluids before hemorrhage was controlled increased the mortality rate, especially if the BP was elevated.
Kowalenko T, Stern S, Dronen S, Wang X. Improved outcome with hypotensive resuscitation of uncontrolled hemorrhagic shock in a swine model. J Trauma 1992;33:349-53. Stern S, Dronen S, Birrer P, Wang X. Effect of blood pressure on hemorrhage volume and survival in a near- fatal hemorrhage model incorporating a vascular injury. Ann Emerg Med 1993;22:155-63.
54. Postulation
* Increased hydrostatic pressure driving ongoing bleeding or dislodging a clot, as well as the decrease in blood viscosity and dilution of clotting factors.
* - Shoemaker WC et al. Resuscitation from severe hemorrhage. Crit Care Med 1996;24:S12-23 .
* A caveat that also bears consideration when comparing such studies, is the anesthetic used, which can also significantly affect blood loss.
* - Soucy DM et al. Effects of anesthesia on a model of uncontrolled hemorrhage in rats. Crit Care Med 1995;23:1528-32.
55. SBP threshold
* Sondeen JL et al. BP at which rebleeding occurs after resuscitation in swine with aortic injury.
* J Trauma 2003;54:S110-7
* Findings: SBP threshold = 90 mmHg, independent of time from start of bleeding.
56.
* Administering large quantities of IV fluids without controlling the hemorrhage results in hemodilution (  HCT,  available Hb (and oxygen- carrying capacity),  clotting factors & ECF compartment
* This effect is found regardless of the fluid used (blood, LR, NS, hypertonic saline).
Hahn RG. The use of volume kinetics to optimize fluid therapy. J Trauma 2003;54:S155-8
57. The optimal volume of IV fluid administered is a balance between improving tissue oxygen delivery against increasing the blood loss by raising SBP MODS CLOTS Major controversy
58. Delayed fluid resuscitation in penetrating trauma
* Bickell WH et al.
* New Engl J Med 1994;331:1105-9.
* Randomized, prospective and blinded comparison of immediate versus delayed fluid resuscitation for hypotensive patients with penetrating torso injuries.
* Methods:
o Patients in the immediate resuscitation group received infusion of isotonic infusion of Ringer's acetate solution through two large bore IV catheters inserted at the scene.
59. Delayed fluid resuscitation in penetrating trauma
o Patients in the delayed resuscitation group also had two large bore IV catheters inserted at the scene but these were then flushed and capped.
* After arrival in the operating room, IV crystalloid and packed red cells were given to all patients to maintain SBP > 100 mm Hg, HCT > 25% and urine output > 50 ml per hour.
* The majority of patients were in hospital within 30 min of reported injury and entered the OR < 1H of hospital time.
60. Delayed fluid resuscitation in penetrating trauma
* 598 studied patients, 70 died before reaching the OR.
* Survival rate of delayed resuscitation group (70%) compared with that in the immediate resuscitation group (62%).
* The frequency of complications was similar in the two groups.
* Conclusion: In hypotensive patients with penetrating torso trauma, delay of fluid resuscitation until operative intervention improves outcome.
61. Regel et al, Acta Anaesthesiol.Scand., 1997
* Data limited to penetrating injuries
* No evidence for blunt haemorrhagic trauma
* Decision on field resuscitation relates to type of trauma and likelihood of hospital transfer
62. On going debate/uncertainty
* Best practice for:
o Penetrating versus blunt trauma
o Rural versus urban settings
o Young versus older patients
o Head injured versus non head injured patients
* ? Malaysian Practice
63. Timing of resuscitation
* Do not delay transfer for resuscitation
* Priority is arrest of hemorrhage
* Commence aggressive resuscitation once control of bleeding is imminent
Pepe et al Emerg.Med Clin.North Am., 1998
64. Pre-hospital resuscitation Søreide & Deakin, Injury, 2005
* Set resuscitation targets according to type of trauma
* • Start isotonic crystalloid infusion
* – Rapid 500ml to achieve targets
* • Reassess after each fluid bolus
* • Do not delay transportation for other than life-saving maneuvers
* • Maintain care during transportation
65. Blunt Trauma Søreide & Deakin, Injury, 2005
* • Goals:
o – Perfusion of vital organs without increasing
o bleeding
* • Minimal fluid resuscitation
o – Rapid infusion of rapid 500ml of isotonic crystalloid
* • Targets:
o – Restore peripheral pulses
o – Keep systolic arterial pressure < 90mmHg
66. TBI Søreide & Deakin, Injury, 2005
* • Goals:
o – Limit bleeding risk
o – Maintain CPP
* • Moderate fluid resuscitation
o – Rapid infusion of rapid 500ml of isotonic crystalloid
* • Targets:
o – Restore and maintain SBP > 110mmHg
67. Penetrating injury Søreide & Deakin, Injury, 2005
* • Goals:
o – Perfusion of at least brain and heart without increasing bleeding
o – Rapid transfer
* • Minimal fluid resuscitation
o – Rapid infusion of 500ml of isotonic crystalloid
* • Targets:
o – Restore basal cerebral perfusion
o – Keep systolic arterial pressure < 80mmHg
68. Søreide & Deakin, Injury (2005) 36, 1001 - 1010
* Fluid resuscitation & blood transfusion in the Emergency Department are still essential elements of the early hospital management of critically ill injured patients
69. Rocha-e-Silva et al. CLINICS 60(2):159-172, 2005
* Review paper: Small volume hypertonic resuscitation of circulatory shock.
* Conclusions:
o Safe, but cautious in moribund, or chronic debilitating diseases.
o First treatment for posttraumatic hypotension, particularly in penetrating trauma head trauma.
o Not a/w increased bleeding, clinically significant hypernatremia and allergic reactions
* Commercially available in European countries.
* A larger prospective, multicenter trials is required to better define the patient population to maximally benefit from hypertonic saline
70.
* SIRS (2 out of 4 criteria) with detection of bacterial focus
* ± /elevated CRP/elevated pro-calcitonin
* Septic shock: sepsis-induced with hypotension despite adequate fluid resuscitation along with the presence of perfusion abnormalities that may include, but not limited to lactic acidosis, oliguria or acute alteration of mental status
Sepsis Crit Care Med 1992;20:864-74
71. Fluids in septic shock Marx et al. Int Care Med , 2002
* • 25 fasted, ventilated pigs
* • Faecal peritonitis
* • Fluid titrated to keep CVP 12mmHg
o – Ringer’s solution (RS)
o – Modified fluid gelatin 4% (MFG4%)
o – Modified fluid gelatin 8% (MFG8%)
o – Hydroxyethyl starch 200/0.5 (HES)
* • Haemodynamics and oxygenation measured at 4 and 8 hours
72. Marx et al. Int Care Med , 2002 Fluid requirements
73. Cardiac output Marx et al. Int Care Med , 2002
74. Mixed S v O 2 Marx et al. Int Care Med , 2002
75. Acid base Marx et al. Int Care Med , 2002
76. Fluids in septic shock Marx et al. Int Care Med , 2002
* Conclusions:
* Colloids were significantly better than Ringer’s for resuscitation in this model
* HES appeared to be slightly better than either isotonic or hypertonic gelatin
77. Sepsis
* • Goals:
o – Restore tissue perfusion rapidly
* • Aggressive fluid resuscitation
o – Rapid infusion of 500ml of isotonic crystalloid and colloid
o – Inotropic support as required
* • Targets:
o – Maintain ScvO2 > 70%
o – Keep systolic arterial pressure > 65mmHg
78. End point of resuscitation
* Traditional: Achieved definitive care
* New: Correction of O 2 debt as end point
79. Prehospital care, Arrival to ED Stabilization of vital signs Relieve tissue hypoxia Admission in ICU Phase 1 Phase 2 Phase 3 End point of Resuscitation of Shock
80. RADY ET AL • RESUSCITATION IN THE ED. AMERICAN JOURNAL OF EMERGENCY MEDICINE • Volume 14, Number 2 • March 1996 . End point of Resuscitation of Shock
81. End point of Resuscitation
82. Davis , Shackford. Base deficit as a guide to volume resuscitation. J. trauma 1988.
o Mild: -2 to -5, moderate: -6 to -14,
o severe: > -14
o Worsening base deficit correlated with ongoing blood loss
o normal base deficit taken as end point of resuscitation
83.
* 76 patients
* Lactate normalized in 24 hr: 100 % survival,
* 24 – 48 hr 78 % survival, > 48 hr: 14 % survivors
* Serum lactate and time to normalization (less
* than or equal to 2 mmol/l) appears to be a
* suitable end point for resuscitation
Abramson et al. Lactate clearance and survival following injury. J. Trauma . 1993
84. Bishop, Shoemaker & colleague J. Trauma 1995
o Prospective randomized trial of survivors values of C.I, O 2 delivery and O 2 consumption as resuscitation end point in severe trauma
o Supranormal values
+ Cardiac Index: CI > 4.5 L/min
+ O 2 Delivery index: DO 2 I > 600ml/min/m2
+ O 2 consumption index: VO 2 I > 170 ml/min/m2
85. Bishop, Shoemaker & colleague J. Trauma 1995
* 50 patients on supranormal variables cf 65 control patients
o lower mortality ( 18 % Vs 37 % )
o fewer organ failures per patient
+ DO 2 I & VO 2 I are strong predictor of multiple organ failure and death
+ Standard hemodynamic measurement MAP, CVP fail to differentiate between survivor and non- survivors.
86. Summary
* Severe hemorrhagic shock
o Aggressive versus judicious fluid therapy (inconclusive)
o Restrictive & permissive hypotension in uncontrolled hemorrhage (clinical evidence is still limited).
o Minimum resuscitation, stop the bleeding (surgical intervention) then maximum resuscitation.
o Future trend may be SVR with HS
o Ringer’s lactate @ NS/ ±Starch is an initial fluid of choice
o Red blood cells if HCT < 25.
o FFP, cryoprecipitate only for coagulation problems
* Septic shock
o Early goal directed, large volume therapy
o Starch is a fluid of choice
87. Conclusions
* Resuscitation should be seen as a continuum in which pre-hospital care, emergency room management and intensive therapy merge.
* Venous access & fluid therapy are a necessary part of this continuum but the optimum timing for fluid administration depends on the circumstances.
* Patient survival is linked to the overall quality, integration, communication & process of care in a trauma system.
88. THANK YOU

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Cause for IHD

Causes for IHD
EAST HAT
1.E-emboli
2.A-atheroma
3.S-Stenosis,Spasm
4.T-thrombosis

5.H-hypertension,hyperthrophy,Hb abnormality
6.A-Anemia
7.T-thyrotoxicosis

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Hydronephrosis

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CANTU

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Ultrasound of Kidney with Hydronephrosis

Ultrasound of Kidney with Hydronephrosis

Hydronephrosis [water - kidney condition] refers to a kidney with a dilated pelvis and collecting system. It can be caused by obstruction of the ureters or bladder outlet. Hydronephrosis can also result from reflux (retrograde leakage of urine from the bladder up the ureters to the renal pelvis. Rarely, some children have hydronephrosis without either obstruction or reflux. This is thought to result form abnormal smooth muscles of the renal pelvis or ureter causing ectasia.

This longitudinal ultrasound of a left kidney shows a large hypoechoic area (black on an ultrasound means no echoes) in the center of the kidney. Notice how the dilation extends into the parenchyma. These areas are the calyces of the kidney. The normal hyperechoic area in the center of the kidney (the hilum) is replaced by a large hydronephrotic renal pelvis. This kidney has hydronephrosis due to obstruction of the upper ureter (additional studies revealed the location of the obstruction).

This longitudinal ultrasound shows a kidney with less severe hydronephrosis. The parenchyma is relatively normal in thickness. The dilation of the collecting system extends from the renal pelvis to the calyces. This is a grade III hydronephrosis.

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Contraindications of activated charcoal = CHARCOAL

Source:http://drcd2009.wordpress.com/

C – caustic/corrosive agents

H – heavy metals

A – alcohols and glycols/absent bowel sounds

R – rapidly absorbed substances

C – cyanide

O – other insoluble drugs/obstructed bowel

A – aliphatic hydrocarbons

L – laxatives

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Aortic Dissection

Percentage	60 %	10-15 %	25-30 %
Type	DeBakey I	DeBakey II	DeBakey III
	Stanford A		Stanford B
	Proximal		Distal
Classification of aortic dissection

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The San Francisco Syncope Rule (CHESS)

The San Francisco Syncope Rule (CHESS)

The criteria demonstrated 96% sensitivity (95% confidence interval [CI], 92% to 100%) and 62% specificity (95% CI, 58% to 66%) for serious outcomes at 7 days

Stickberger SA, Benson W, Biaggioni I, et al. AHA/ACCF scientific statement on the evaluation of syncope. J Am Coll Cardiol. 2006;12:473-484

Caution:

Up to 11% of patients discharged home with 0 out of 5 on the “CHESS” algorithm may still have a serious outcome as defined in the study within 30 days — an unacceptably high risk

Miller CD, Hoekstra JW. Prospective validation of the San Francisco Syncope Rule: Will it change practice [Editorial]? Ann Emerg Med. 2006;47:455-456

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Ankle Block

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Wrist Block

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Canadian C-Spine Rule

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AAA

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Aortic Aneurysm

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Canadian CT Head Rule

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MI-Classes

A 2007 consensus document classifies myocardial infarction into five main types:

* Type 1 - Spontaneous myocardial infarction related to ischaemia due to a primary coronary event such as plaque erosion and/or rupture, fissuring, or dissection
* Type 2 - Myocardial infarction secondary to ischaemia due to either increased oxygen demand or decreased supply, e.g. coronary artery spasm, coronary embolism, anaemia, arrhythmias, hypertension, or hypotension
* Type 3 - Sudden unexpected cardiac death, including cardiac arrest, often with symptoms suggestive of myocardial ischaemia, accompanied by presumably new ST elevation, or new LBBB, or evidence of fresh thrombus in a coronary artery by angiography and/or at autopsy, but death occurring before blood samples could be obtained, or at a time before the appearance of cardiac biomarkers in the blood
* Type 4 - Associated with coronary angioplasty or stents:
o Type 4a - Myocardial infarction associated with PCI
o Type 4b - Myocardial infarction associated with stent thrombosis as documented by angiography or at autopsy
* Type 5 - Myocardial infarction associated with CABG

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Cranial Nerves

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Brain Herniation

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Intracranial contusion

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Decorticate/Decerebrate Position

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Intracerebral hematoma

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Subdural Hematoma

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Subdural/Extradural Hematoma

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Acromioclavicular Joint Injury

Source:http://emedicine.medscape.com/article/92337-overview


Introduction

Injuries in and around the shoulder are common in today's athletic society. Proper knowledge of the different problems and treatment options for shoulder disorders is necessary to get patients back to their preinjury state.

Background

Acromioclavicular (AC) joint injuries are common and often seen after bicycle wrecks, contact sports, and car accidents. The acromioclavicular joint is located at the top of the shoulder where the acromion process and the clavicle meet to form a joint. Several ligaments surround this joint, and depending on the severity of the injury, a person may tear one or all of the ligaments. Torn ligaments lead to acromioclavicular joint sprains and separations.1

The distal clavicle and acromion process can also be fractured. Injury to the acromioclavicular joint may injure the cartilage within the joint and can later cause arthritis of the acromioclavicular joint.

This article discusses the anatomy of the acromioclavicular joint, the diagnosis of disorders of this joint, and the different treatment options.

For excellent patient education resources, see eMedicine's Breaks, Fractures, and Dislocations Center. Also, see eMedicine's article on Shoulder Dislocation.

Related eMedicine topics:
Acromioclavicular Injury [in the Emergency Medicine section]
Acromioclavicular Joint Separations [in the Orthopedic Surgery section]
Dislocation, Shoulder [in the Emergency Medicine section]
Shoulder Dislocation [in the Orthopedic Surgery section]
Frequency
United States

Injuries to the acromioclavicular joint are the most common reason that athletes seek medical attention following an acute shoulder injury. Glenohumeral dislocations (see Shoulder Dislocation) are the second most common injuries seen. Men in their second through fourth decades of life have the greatest frequency of acromioclavicular joint injuries, which are most often incomplete tears of the ligaments.1
Functional Anatomy

The normal width of the acromioclavicula joint is 1-3 mm in younger individuals; it narrows to 0.5 mm or less in individuals older than 60 years.

The acromioclavicular joint is made up of 2 bones (the clavicle and the acromion), 4 ligaments, and a meniscus inside the joint.

* The acromioclavicular joint is surrounded by a thin joint capsule and 4 small ligaments. These ligaments mostly give joint stability to anterior and posterior translation, as well as provide horizontal stability to the joint.
* Another set of ligaments also provides vertical stability to the acromioclavicular joint. These ligaments are called the coracoclavicular ligaments, which are found medial to the acromioclavicular joint and go from the coracoid process on the scapula to the clavicle.
* Different injuries result in different tears of the 2 coracoclavicular ligaments (the conoid and the trapezoid). Torn acromioclavicular joint ligaments and/or torn coracoclavicular ligaments are seen in acromioclavicular joint sprains. The meniscus that lies in the joint may also be injured during sprains or fractures around the acromioclavicular joint.
o The acromioclavicular capsular ligaments provide most of the joint stability in the anteroposterior (AP) direction. The conoid and trapezoid ligaments aid in providing superior-inferior stability to the joint. Compression of the joint is restrained mainly by the trapezoid ligament.

Sport-Specific Biomechanics

When a person falls onto their shoulder, the force pushes the tip of the shoulder down. The clavicle is usually kept in its anatomic position, whereas the shoulder is driven down, which injures the different ligaments or causes a fracture. When the ligaments are injured they are either sprained or, in more severe cases, torn.

Acromioclavicular joint sprains have been classified according to their severity. In a type I sprain, a mild force applied to these ligaments does not tear them. The injury simply results in a sprain, which hurts, but the shoulder does not show any gross evidence of an acromioclavicular joint dislocation. Type II sprains are seen when a heavier force is applied to the shoulder, disrupting the acromioclavicular ligaments but leaving the coracoclavicular ligaments intact. When these injuries occur, the lateral clavicle becomes a little more prominent.

In type III sprains, the force completely disrupts the acromioclavicular and coracoclavicular ligaments. This leads to complete separation of the clavicle and obvious changes in appearance. The lateral clavicle is very prominent. A few more types of acromioclavicular joint sprains have been classified, but types I–III are the most common (see Image 1 or below).

Classification of acromioclavicular joint injurie...
Classification of acromioclavicular joint injuries.

[ CLOSE WINDOW ]

Classification of acromioclavicular joint injurie...

Classification of acromioclavicular joint injuries.


An acromioclavicular joint sprain is more common than a fracture after an injury. However, fractures of the distal clavicle and the acromion process may occur, so the healthcare provider must be aware of such injuries and ready to diagnose and treat them as well (see Clavicular Injuries).
Clinical
History

An acromioclavicular joint injury should be considered in any patient complaining of pain over the superior part of the shoulder. Injuries to this part of the body are painful.

* The most common mechanism for an acromioclavicular joint injury is a fall directly onto the acromion, with the arm adducted up against the body. Multiple indirect forces can result in an acromioclavicular joint injury. A fall onto an outstretched hand (FOOSH injury) and a downward force on the upper extremity have been implicated in acromioclavicular joint injuries.1,2,3
* In the immediate setting, the patient may initially experience generalized shoulder tenderness and swelling; however, as the diffuse pain resolves, specific point tenderness over the acromioclavicular joint is usually noted. The athlete may note a significant abrasion or prominence of the distal clavicle.
* Athletes involved in weight training typically experience pain with specific exercises such as with use of the bench press and dips.
* Many individuals experience nocturnal pain and awakening when rolling onto the involved shoulder, which puts pressure on the acromioclavicular joint.
* Rarely, the patient may report popping or catching in the region of the acromioclavicular joint.

Physical

* Patients have pain over the acromioclavicular joint. Swelling, bruising, and a prominent clavicle may be evident, depending on the type of sprain that the patient has sustained. In types I and II sprains, deformity is usually minimal. In type III, the distal clavicle is abnormally prominent. Of note, clavicle fractures, without acromioclavicular joint sprains, can also cause the clavicle to be prominent.
* The patient has poor shoulder range of motion and moderate pain when trying to raise up the arm.
* In the acute situation, the examiner may have difficulty ruling out a concomitant rotator cuff tear, as active and passive shoulder abduction maneuvers are difficult to perform in the face of an acromioclavicular joint separation.
* The most reliable physical examination test for acromioclavicular joint pathology is the cross-body adduction test. The test is performed by elevating the arm on the affected side 90º, while the examiner grasps the elbow and adducts the involved arm across the body. Although reproduction of pain with this maneuver may occur in patients with posterior capsule tightness or subacromial impingement, pain is suggestive of acromioclavicular joint pathology. Restriction of range of motion, which is rarely associated with acromioclavicular joint pathology, more likely suggests adhesive capsulitis or glenohumeral arthritis.

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Kernohan's notch

From Wikipedia, the free encyclopedia

Kernohan's notch is a cerebral peduncle indentation associated with some forms of transtentorial herniation.^[1][2] It is a secondary condition caused by a primary injury on the opposite hemisphere of the brain.^[3] Kernohan's notch is an ipsilateral condition, in that a left-sided primary lesion (in which Kernohan's notch would be on the right side) evokes motor impairment in the left side of the body and a right-sided primary injury evokes motor impairment in the right side of the body.^[4] The seriousness of Kernohan's notch varies depending on the primary problem causing it, which may range from benign brain tumors to advanced subdural hematoma.

Contents 1 Mechanism 2 Causes 3 Signs and symptoms 4 Diagnosis 5 Treatments 6 Case studies 6.1 Kernohan's notch and misdiagnosis 6.2 Left ruptured occipital arteriovenous malformation 7 History 7.1 Early findings 7.2 Kernohan-Woltman 8 See also 9 Notes 10 References

Mechanism

Kernohan's notch phenomenon is a result of the compression of the cerebral peduncle, which is part of the mesencephalon, against the tentorium due to transtentorial herniation. This produces ipsilateral hemiparesis or hemiplegia^[5]

The skull is an in compressible closed space with a limited volume (Monro-Kellie Doctrine). When there is increased cranial pressure in the brain, a shift in the brain forms towards the only opening of the skull, the foramen magnum. Thus, when an increase of pressure in a hemisphere of the brain exists, the cerebral peduncle on the opposite hemisphere is pushed up against the tentorium, which separates the posterior fossa from the anterior fossa. This produces a visible "notch" in the cerebral peduncle.^[6] Because of the fact that a Kernohan's notch is caused by an injury creating pressure on the opposite hemisphere of the brain, it is characterized as a false localizing sign.^[7]

The Kernohan's notch phenomenon is unique in that it is not only a false localizing sign, but is also ipsilateral or same-sided. The left cerebral peduncle contains motor fibers that cross over to the right side of the body. Thus, if you have a right hemisphere problem, it causes a Kernohan's notch in the left cerebral peduncle which results in right-sided motor impairment. Therefore you get, paradoxically, impairment of motor function on the same side of the body as the injury causing the Kernohan's notch.^[8]

Causes

The Kernohan's notch is a secondary phenomenon that results from a major primary injury. Non-tumoral, non-traumatic, intracranial haemorrhage rarely causes this phenomenon.

A wide range of serious injuries can cause an increase in intracranial pressure to trigger the formation of a Kernohan's notch. In general, this phenomenon occurs in patients with advanced brain tumor or severe head injury.^[9] In the case of severe head injury, a clot can occur over the surface of the brain and can often cause shift of the middle part of the brain against the tentorium, which creates the Kernohan's notch. Chronic subdural hematomas have been known to be a familiar cause of Kernohan's notch.^[10]

MRIs have shown evidence of Kernohan's notch from patients with traumatic head injury that are related to acute space-occupying lesions such as subdural hematoma, epidural hematoma, depressed skull fracture, or spontaneous intracerebral hematoma.^[11][12]

Also, it is important to note that the anatomical size of tentorial notches vary considerably between individuals; however, very little evidence supports that a more narrow notch creates a predisposition towards Kernohan's notch.^[13]

Signs and symptoms

Symptoms directly related to the Kernohan's notch is most commonly paralysis or weakness on one side of the body.^[14] Paralysis and weakness is known as hemiplegia and hemiparesis, respectively. This is due to destruction or pressure applied to the motor fibers located in the cerebral peduncle. A more rare sign of Kernohan's notch is ipsilateral oculomotor nerve palsy.^[15]

However, most patients come into the clinic citing symptoms associated with the primary injury causing the Kernohan's notch. Since so many types of head injuries exist, virtually any symptom of brain trauma can be seen accompanying Kernohan's notch. These symptoms may range from total paralysis to simple headache, nausea, and vomiting.^[16]

Diagnosis

Because of the ipsilateral characteristic of Kernohan's notch, diagnosis is unique. Many clinicians assume a right sided paralysis corresponds with an injury in the left hemisphere of the brain and misdiagnose Kernohan's notch.^[17] Despite this complication that ipsilateral paralysis causes, it makes it very easy to diagnose when coupled with imaging techniques. For example, when seeing an MRI of a blood clot on the left side of the brain coupled with left-sided paralysis, it immediately points to Kernohan's notch.

In most head trauma cases, CT scans are the standard diagnostic method; however it is not ideal for imaging small lesions, so MRI is used to identify Kernohan's notch. It is important to distinguish Kernohan's notch from direct brain stem injuries. Case studies have shown that in patients with chronic subdural hematoma, a compressive deformity of the crus cerebri without an abnormal MRI signal may predict a better recovery in patients with Kernohan's notch.^[18]

Treatments

There is no special treatment for Kernohan's notch since treatment is completely dependent on the injury causing it. The pressure against the tentorium should be relieved and the notch should go away. However, this does not mean that damage to the motor fibers disappears. Depending on the severity of the injury, there may or may not be persistent damage after pressure relief. Neurological deficits may resolve after surgery, but some degree of deficit, especially motor weakness, generally remains.^[19]

Pressure relief to "un-notch" the cerebral peduncle may include the removal of brain tumors and blood clots or the suction of blood from a drilled hole in the skull.^[20]

Case studies

Kernohan's notch and misdiagnosis

The ipsilateral and false localizing signs characteristic of Kernohan's notch sometimes cause confusion and result in misdiagnosis. Such a case is described in an account by Wolf at the University Hospital in Groningen, Netherlands^[21]:

"A 39 year-old man sustained a minor head injury when he was struck on the head by a golf club. 5 hours later, he had sudden onset of headache with nausea and vomiting, Simultaneously he developed muscle weakness on his left side. He then became somnolent. A CT scan showed a subdural blood collection on the left side...these findings puzzled the attending neurologist as well as the radiologist who both expected the abnormalities to be on the opposite (right) side. The radiological technician remarked that the left-right marks were not in the usual place on the monitor screen and argued that the latest scan had been a coronal infundibulum scan in which a top-view is used instead of a bottom view...It was then decided that the patient had a right-sided acute subdural haematoma. In the operating room a right-sided drilling hole was made but no blood was aspirated, nor was it from a second right-sided drilling hole. A right-sided craniotomy was then done, which did not show any signs of a subdural blood collection and the operation was ended...a postoperative CT scan the next day showed a subdural haematoma on the left side and the signs of craniotomy on the right...Reconstruction of the events led to the conclusions that the false localizing signs were caused by a Kernohan notch...the left-right marks on the screen had initially been correct but were wrongly switched to fit the patients' clinical symptoms. This sad, but unique, example of misdiagnosis has prompted us to re-evaluate the index settings before examination of each new patient."

Left ruptured occipital arteriovenous malformation

Kernohan's notch phenomenon associated with a ruptured arteriovenous malformation (AVM) is rare, but not unknown. This was accounted for in a case study described by Fujimoto at the Tsukuba Memorial Hospital in Ibaraki, Japan^[22]:

"The patient, a 23 year-old woman, visited our outpatient clinic with a chief complaint of severe headache, nausea and vomiting. Her pupils did not react to light and her left pupil was mydriasic...The patient was immediately operated on to decompress the brain and remove the subdural hematoma. The onset-operation interval was 46 min...Intraoperatively, a parenchymal AVM was found in the occipital area, which was removed. On day four part onset, we noticed left hemiparesis with a partial left oculomotor nerve palsy, the so called Kernohan's phenomenon...One month after onset, the patient had no significant neurological deficit...We believe that her good outcome with little neurological deficit was due to the short interval from onset to the first operation."

History

Early findings

One of the first references to casual brain herniation was that of James Colier, who clearly described cerebellar tonsilar herniation in 1904.^[23] He observed accompanying false localyzing signs and commented:

"In many cases of intracranial tumour of long duration, it was found postmortem that the posterior inferior part of the cerebellum had been pushed down and backwards into the foramen magnum and the medulla itself somewhat cadually displaced, the two structures together forming a cone-shaped plug tightly filling up the foramen magnum."

In 1920, Adolf Meyer confirmed the pathologies of brain herniation.^[24] He commented:

"The falx and tentorium constitute an important protection against any sudden impacts of pressure by keeping apart heavy portions of the brain, but they also provide an opportunity for trouble in case of swelling or need of displacement."

The work of Collier and Meyer described ipsilateral hemiparesis, a false localizing sign. However, it became known as the Kernohan-Woltman phenomenon.^[25]

Kernohan-Woltman

In 1929, Kernohan and Woltman published their work on brain lesions that showed ipsilateral hemiplegia.^[26] In their paper, they state:

"The tumour was often large enough to displace the brain toward the opposite side and also to cause herniation through the tentorium. Such herniation and displacement may be evidenced by a groove sweeping over the uncinate gyrus on the side of the tumour. On the opposite side the groove may be absent...".(p. 282)

Kernohan fully described the Kernohan's notch in 1929 and is given credit for its discovery.

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Tentorium Cerebelli

From Wikipedia, the free encyclopedia

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Brain: Tentorium cerebelli
Tentorium cerebelli seen from above.
	subject #193 874
	Meninges
	ancil-261

The tentorium cerebelli or cerebellar tentorium (Latin: "tent of the cerebellum") is an extension of the dura mater that separates the cerebellum from the inferior portion of the occipital lobes.

Anatomy

The tentorium cerebelli is an arched lamina, elevated in the middle, and inclining downward toward the circumference.

It covers the superior surface of the cerebellum, and supports the occipital lobes of the brain.

Its anterior border is free and concave, and bounds a large oval opening, the incisura tentorii, for the transmission of the cerebral peduncles.

It is attached, behind, by its convex border, to the transverse ridges upon the inner surface of the occipital bone, and there encloses the transverse sinuses; in front, to the superior angle of the petrous part of the temporal bone on either side, enclosing the superior petrosal sinuses.

At the apex of the petrous part of the temporal bone the free and attached borders meet, and, crossing one another, are continued forward to be fixed to the anterior and posterior clinoid processes respectively.

To the middle line of its upper surface the posterior border of the falx cerebri is attached, the straight sinus being placed at their line of junction.

Clinical significance

Clinically, the tentorium is important because brain tumors are often characterized as supratentorial (above the tentorium) and infratentorial (below the tentorium). The location of the tumor can help in determining the type of tumor, as different tumors occur with different frequencies at each location. Additionally, most childhood tumors are infratentorial, while most adult tumors are supratentorial. The location of the tumor may have prognostic significance as well.

Since the tentorium is a hard structure, if there is a volume expansion in the parenchyme above the tentorium, the brain can get pushed down partly through the tentorium. This is called herniation and will often give mydriasis on the affected side, due to pressure on cranial nerve III (N. Oculomotorius). Tentorial herniation is a serious symptom, especially since the brainstem is likely to be compressed as well if the intracranial pressure rises further.

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