Epidural/Extradural Hematoma

Extradural/Epidural hematoma

Definition

Epidural hematoma (EDH) is a traumatic accumulation of blood between the inner table of the skull (calvaria) and the stripped-off periosteal layer of dura membrane. It can also occur in the spinal cord (spinal epidural hematoma-SEDH).

Incidence and Prevalance

United States

Epidural hematoma complicates 2% of cases of head trauma

Mortality/Morbidity

Mortality rate associated with epidural hematoma has been estimated to be 5-50%.

Pathophysiology

Usually traumatic in nature; associated with calvarial fractures. Epidural hematoma usually results from a brief linear contact force to the calvaria that causes separation of the periosteal dura from bone and disruption of interposed vessels due to shearing stress.

Common arterial sources

70-80% of epidural hematomas (EDHs) are located in the temporoparietal region and the middle meningeal artery are involved most commonly (66%), although the anterior ethmoidal artery may be involved in frontal injuries.

Common venous sources

Usually, venous epidural hematomas only form with a depressed skull fracture.

Torn venous sinuses cause an epidural hematoma, particularly in the parietal-occipital region or posterior fossa (eg, transverse or sigmoid sinus). Hematoma in the posterior fossa represent only 5% of cases.. Disruption of the superior sagittal sinus may cause vertex EDH.

Etiology

· Traumatic

· Thrombolysis/anticoagulants

· Hypertension

Presentation

Symptoms of epidural hematoma include the following:

• Headache
• Nausea/vomiting
• Seizures
• Focal neurologic deficits (eg, visual field cuts, aphasia, weakness, numbness)

The physical examination should include a thorough evaluation for evidence of traumatic sequelae and associated neurological deficits, including the following:

• Bradycardia and/or hypertension indicative of elevated intracranial pressure
• Cerebrospinal fluid (CSF) otorrhea or rhinorrhea resulting from skull fracture with disruption of the dura
• Hemotympanum
• Instability of the vertebral column
• Alteration in level of consciousness (ie, Glasgow Coma Scale score)

• Anisocoria (eg, ipsilateral dilation of the pupil due to uncal herniation with compression of the oculomotor nerve)
• Facial nerve injury
• Weakness (eg, contralateral hemiparesis due to compression of the cerebral peduncle)
• Other focal neurological deficits (eg, aphasia - Aphasia is an acquired disorder of language due to brain damage., visual field defects, numbness, ataxia - Ataxia is defined as an inability to maintain normal posture and smoothness of movement.)

Investigation

Laboratory test

• Complete blood count (CBC) with platelets - To monitor for infection and assess hematocrit and platelets for further hemorrhagic risk.
• Prothrombin time (PT)/activated partial thromboplastin time (aPTT) - To identify bleeding diathesis. bleeding diathesis is an unusual susceptibility to bleeding
• Serum chemistries, including electrolytes, blood urea nitrogen (BUN), creatinine, and glucose - To characterize metabolic derangements that may complicate clinical course.
• Toxicology screen and serum alcohol level - To identify associated causes of head trauma and establish need for surveillance with regard to withdrawal symptoms.
• Type and hold an appropriate amount of blood - To prepare for necessary transfusions needed because of blood loss or anemia.

Imaging test

Plain radiography

CT scan. Advantage is that both fracture and the hematoma are visible.

Angiography – to visualise any lacerated vessels

MRI

Treatment and Management

Emergency care

 Establish IV access, administer oxygen, monitor, and administer IV crystalloids(normal saline) as necessary to maintain adequate blood pressure.

 Intubate using rapid sequence induction (RSI), to facilitate oxygenation, protect the airway, and allow for hyperventilation as needed.

 Elevate head of the bed 30° after the spine is cleared, to reduce ICP and increase venous drainage.

 Administer mannitol(Mannitol is used clinically to reduce acutely raised intracranial pressure until more definitive treatment can be applied). This reduces both ICP (by osmotically reducing brain edema) and blood viscosity, which increases cerebral perfusion.

 Hyperventilation to partial pressure of carbon dioxide (PCO₂) of 30-35 mm Hg treats signs of increasing ICP. This procedure reduces ICP by hypocarbic vasoconstriction and reduces risks of hypoperfusion and death of injured cells.

 Phenytoin reduces the incidence of early posttraumatic seizures, although it does not affect late-onset seizures or the development of a persistent seizure disorder.

Operative care

Craniotomy or laminectomy is followed by evacuation of the hematoma, coagulation of bleeding sites, and inspection of the dura. The dura is then tented to the bone.

Mininally invasive techniques involve the use of burr holes and drainage by negative pressure.

Burr holes procedure: The surgeon will make an incision, and reflect the scalp over the area of the hematoma. Then, an air powered drill is used to make a hole in the skull. The dura mater (tough covering of the brain) is then opened. The hematoma (blood clot) is now seen, and the surgeon will irrigate some of it out, and may pass a drain around the brain to provide post-operative drainage

References
www.emedicine.medscape.com

Solutions

Dextrose Solution (D5W) 5%
Pharmacological Effects
• Provides calories for some metabolic needs. Each 100 mL provides 5 gm of Dextrose. Depending on the presence of insulin, glucose enters cells and is broken down to pyruvate. With adequate oxygen, it enters the Kreb's cycle in the mitochondria and is converted into energy (A.T.P.), CO2 and H2O. The brain and gonads do not require insulin for glucose metabolism.
• Supplies body water for hydration.
• Spares body protein by providing carbohydrate for metabolism.
• Osmolarity of D5W is 252 mOsm/L. The fluid is isotonic when in the container. After administration, the dextrose is quickly metabolized in the body, leaving only water - a hypotonic fluid.
• The pH range is 3.5 - 6.5.
• Capable of producing diuresis depending on clinical state of the patient.
• Also used as diluent.

Side Effects
• Hyperglycemia. Include thirst, increased urination, confusion, drowsiness, flushing, rapid breathing, and fruity breath odor
• Fluid overload. Swelling of ankles/feet.
• Symptoms of a serious allergic reaction may include: rash, itching, swelling, severe dizziness, trouble breathing.

Contraindications
• Patients at risk for increased intracranial pressure.
• Patients who have an acute neurological dysfunction.
• Hypovolemic states.
• Patients at risk for third-space fluid shifts.
• Elevated blood glucose concentrations.

0.9% Saline Solution
Side Effects
• Metabolic acidosis when administered in sufficiently large quantities.
• Fluid overload. Swelling of ankles/feet.

Contraindications
• heart problems (e.g., congestive heart failure)
• lung problems (pulmonary edema)
• kidney problems
• low levels of potassium (hypokalemia)
• high levels of sodium (hypernatremia)
• swelling (edema)
• allergies.

Hartmann Solution – Sodium Lactate (different from ringer solution, uses bicarbonate)
Side Effects
• Contains Ca++ and this can cause problems if administered with stored blood. Citrate=anticoagulant (Ca++ dissolves citrate causes lost of anti-coagulablity)
• Fluid overload. Swelling of ankles/feet.
• Symptoms of a serious allergic reaction may include: rash, itching, swelling, severe dizziness, trouble breathing.

Contraindications
• Hartmann's solution is said to be contraindicated in patients with diabetes mellitus, as one of the isomers of lactate is gluconeogenic

Fluid Management - Part I (water balance, osmolarity, tonicity)

Water Balance :
- The total amount of fluid or water is called the total body water, which accounts for 50% to 70% of body weight.
o Eg. 70 kg man whose total body water is 65% of his body weight has 45.5 L of water.
- Total body water correlates inversely with body fat. Eg. More total body water, lower body fat, vice versa.
- Total body water is distributed between 2 major body fluid compartments: intracellular fluid (ICF) and extracellular fluid (ECF)
o ECF (1/3 of total body fluid)
- Plasma
- Interstitial fluid
o ICF (2/3 of total body fluid)
- Fluid within the cells


Site of water loss :
- Skin
- Urinary tract
- Gastrointestinal
- Respiratory airway

Daily intake of water :
- Ingested in the form of liquids or water in the form of food.
- Synthesized in the body as a result of oxidation of carbohydrate.

Daily loss of water :
• Insensible loss
• Minimal sweat loss
• Faecal loss
• Minimal urine volume to excrete solute load: 500 mls

Osmolarity :
- Osmole – number of particles into which a solute dissociates in solution
- Osmolarity - concentration of osmotically active particles in solution expressed as osmoles per litre.
- It is necessary to know the conc. Of solute and whether the solute dissociates in the solution.
- Eg. Glucose does not dissociate in solution, osmolarity = molarity
- Eg. NaCl dissociates into 2 particles, osmolarity x number of particles in solution
- Osmolarity = g C
o g- number of particles per mole in solution (Osm/mol)
o C – Concentration (mmol/L)

Electroneutrality of body fluid compartments :
- Each body fluid compartment must obey the principle of electroneutrality
o Each compartment must have the same conc. In mEq/L of positive charges (cations) as of negative charges (anions)
o ECF : cation, Na+ / balancing anions, Cl- and HCO3-
o ICF : cation, K+ and Mg2+ / balancing anions, proteins and organic phosphate
o Conc. Differences for individual solutes, the total solute conc. (osmolarity) is the same in ICF and ECF, equality is achieved because water flows freely across cell membranes.
- Water intake in excess of requirements is excreted as urine.
- As daily solute load increases, the maximum urine osmolality decreases until, at high solute loads, it is the same as plasma osmolality.
o This occurs because the increased urine flows necessary to carry the increased solute washes out the medullary osmoles and the time spent in the tubules is decreased.

Tonicity :
- Tonicity refers to the ability of a solution to affect the fluid content and pressure of cells.
- An isotonic solution has the same effective osmolarity of about 300mOsm as intracellular fluid and would not cause any net movement of water in or out of cells.
o A 0.9% solution of sodium chloride (150mM), generally known as normal saline, is an isotonic solution and causes no change in cell volume or shape.
- A hypotonic solution has a lower osmolarity than intracellular fluid, and this would cause water to move into the cells by osmosis.
- A hypertonic solution such as sea water has more non-permeating solutes than intracellular fluid and causes cells to lose water and shrivel or crenate (take on a spikey appearance).
- Water moves so freely through cell membranes by osmosis such that osmotic equilibrium is established within less than a minute after ECF osmolarity first deviates from normal.

Investigations and Treatment for Hyponatremia

Investigations

• The diagnosis of hyponatremia: Concentration of sodium in serum
• There may be errors for eg, if sample obtained from site just proximal to infusion of hypotonic saline/ dextrose in water
• Hyperglycemia may lead to low serum sodium levels but it isn’t a true hyposmolar state, as hyperglycemia causes a shift of free water from intracellular to extracellular space thereby diluting the sodium (by a factor of 1.6 mEq/L for each 100 mg/dL increase above normal serum glucose concentration). Concentration resumed once normoglycemia re-established.
• Hyponatremia may be noted in patients whose serum contains unusually large quantities of protein or lipid.
o In these patients, an expanded plasma protein or lipid fraction leads to a decrease in the plasma water fraction in which sodium is dissolved.
o Laboratory techniques that measure absolute sodium content per unit of plasma water report low sodium levels despite the fact that the concentration of sodium in serum water remains within the normal range.
o This phenomenon is known as pseudohyponatremia,
o Hyperlipidemia that is severe enough to produce pseudohyponatremia almost always is accompanied by a notably lipemic appearance of the serum sample.
o Hyperproteinemia of sufficient magnitude to induce pseudohyponatremia commonly is due to coexisting multiple myeloma.

Serum osmolarity: Helpful in establishing the diagnosis of true hyposmolar hyponatremia. Serum osmolarity is abnormally low in patients with hyposmolar hyponatremia, but it is normal in patients with pseudohyponatremia due to hyperlipidemia or hyperproteinemia and normal or elevated in patients with hypertonic hyponatremia due to serum hyperglycemia.

Urine sodium levels
• Hypovolemic hyponatremia: Non-renal: Vomiting, diarrhea, fistulas, GI drainage and third spacing of fluids have avid renal absorption of tubular sodium and urine sodium levels of less than 20 mEq/L. Renal: Diuretics, salt-losing nephropathy and aldosterone deficiency have elevated urine sodium levels in excess of 20 mEq/L.
• Hypervolemic hyponatremia: Non-renal: decrease in circulating volume (eg, cirrhosis, nephrosis, congestive heart failure) have urine sodium levels of less than 20 mEq/L. Renal: (SIADH) have urine sodium levels in excess of 20 mEq/L.

Urine osmolarity may be helpful in establishing the diagnosis of SIADH. Typically, patients with SIADH have inappropriately concentrated urine, with urine osmolarities in excess of 100 mOsm/L. Other forms of hyponatremia doesn’t result in such concentrated urine (normal ADH levels)

Serum thyroid-stimulating hormone (TSH) and free thyroxin levels should be checked if the clinical presentation is consistent with hypothyroidism.

Adrenal function should be assessed, via random serum cortisol levels or adrenocorticotropic hormone (ACTH) stimulation test, in patients who have recently taken oral steroids or in any patient suspected of having cortisol deficiency.

Serum ADH levels are not routinely used in the evaluation of hyponatremia because the assay is technically difficult and not widely available on a stat basis. Recently, a serum peptide known as copeptin has been studied in the evaluation of hyponatremia. Copeptin is the C terminal portion of provasopressin and is released in equimolar amounts with vasopressin (ADH).

Imaging Studies: A head CT scan is indicated in patients with altered mental status to ensure that no other underlying cause for the mental status is present.

Treatments

Emergency Care
• Supply O2 and IV glucose in hypoglycaemic patients who exhibit lethargy.
• Anticonvulsant therapy to patients experiencing seizures but if it is secondary to hyponatremia, unlikely to respond but still should do it until diagnosis is made.
• Intubate and initiate hyperventilation to reduce intracranial pressure in patients exhibiting signs of brainstem herniation (eg: fixed, unilateral, dilated pupil; decorticate posturing) until a more definitive therapy can be initiated.
• Avoid giving hypotonic intravenous fluids because they may exacerbate cerebral edema.

Acute hyponatremia (less common)
• Typically is seen in patients with a history of sudden free water loading (eg, patients with psychogenic polydipsia, infants fed tap water for 1-2 d, patients given hypotonic fluids in the postoperative period).
• Acute evolution of hyponatremia leaves little opportunity for compensatory extrusion of CNS intracellular solutes.
• The ultimate danger for these patients is brainstem herniation when sodium levels fall below 120 mEq/L.
• The therapeutic goal is to increase the serum sodium level rapidly by 4-6 mEq/L over the first 1-2 hours.
• The source of free water must be identified and eliminated.
• In patients with healthy renal function and mild to moderately severe symptoms, the serum sodium level may correct spontaneously without further intervention.
• Patients with seizures, severe confusion, coma, or signs of brainstem herniation should receive hypertonic (3%) saline to rapidly correct serum sodium level toward normal but only enough to arrest the progression of symptoms. An increase in serum sodium level of 4-6 mEq/L is generally sufficient. Any further correction is potentially dangerous and must be avoided unless necessary to correct continued seizures or other severe CNS abnormality.

Chronic hyponatremia (more common)
• Patients with mild symptoms and a serum sodium level of 125 mEq/L or less often have chronic hyponatremia. These patients lack any history of sudden free water loading.
• Chronic hyponatremia must be managed with extreme care; treatment of chronic hyponatremia has been associated with the development of the osmotic demyelination syndrome characterized by focal demyelination in the pons and extrapontine areas associated with serious neurologic sequelae.
• Management should include meticulous attention to adequate oxygenation and a gradual increase in serum sodium level to 120-125 mEq/L. Serum sodium level should not be allowed to reach normal levels or hypernatremic levels within the first 48 hours.
• The risk of osmotic demyelination appears to be minimal in patients whose chronic hyponatremia is corrected at a rate not to exceed 10-12 mEq/L in the first 24 hours and not to exceed 18 mEq/L in the first 48 hours
• Patients with chronic hyponatremia and severe symptoms (eg, severe confusion, coma, seizures) should receive hypertonic saline but only enough to raise the serum sodium level by 4-6 mEq/L and to arrest seizure activity.
o Further correction should proceed at an overall rate that is no greater than 10-12 mEq/L in the first 24 hours and no greater than 18 mEq/L in the first 48 hours.

• In treating patients with chronic hyponatremia and mild to moderately severe symptoms, consider the cause of the hyponatremic state. Patients are classified as having hypovolemic, euvolemic, or hypervolemic hyponatremia based on historical clues and physical examination. Regardless of the therapeutic approach, serum sodium must be monitored closely and corrected no faster than 10-12 mEq/L in the first 24 hours and 18 mEq/L in the first 48 hours.
o Hypovolemic hyponatremia: Patients have decreased total body sodium stores. If symptoms are mild to moderately severe, treat with isotonic saline; monitor serum sodium levels frequently to ensure that the serum sodium level increases slowly.
o Hypervolemic hyponatremia: Patients have increased total body sodium stores. Treatment consists of sodium and water restriction and attention to the underlying cause. The vasopressin receptor antagonists conivaptan (Vaprisol) and tolvaptan (Samsca) are used in hospitalized patients with hypervolemic hyponatremia.
o Euvolemic hyponatremia: This implies normal sodium stores and a total body excess of free water. Treatment consists of free water restriction and correction of the underlying condition. Recently developed AVP (vasopressin) receptor antagonists (eg, conivaptan, tolvaptan) show promise as effective and well-tolerated intravenous therapy for SIADH. Further studies are needed to better define their role in the treatment of hyponatremia associated with SIADH

Hypertonic Saline
Sodium Requirement (mEq) = TBW (Desired Na - Serum Na) where TBW = Body Weight X 0.6

Volume of Hypertonic Saline = Na Requirement (mEq) X 1000 / Infusate Na Concentration (mEq/L)

For example, a 60-kg woman with serum sodium level of 113 mEq/L would require 280 mL of hypertonic saline in order to increase serum sodium by 4 mEq/L (could be administered as 140 mL/h for 2 h)

In general, 200-400 mL of 3% NaCl is reasonable dose in most adult patients with severe symptomatic hyponatremia
Give IV over first 1-2 h until resolution of seizures or herniation

Arginine vasopressin antagonists (Conivaptan: non-selective, Tolvaptam: selective)
These agents treat hyponatremia through V2 antagonism of AVP in the renal collecting ducts. This effect results in aquaresis (excretion of free water).

Arginine vasopressin antagonist Conivaptan (V1A, V2) indicated for euvolemic and hypervolemic hyponatremia. Increases urine output of mostly free water, with little electrolyte loss.

Selective vasopressin V2 -receptor antagonist Tolvaptam, indicated for hypervolemic and euvolemic hyponatremia (i.e., serum sodium level <125 mEq/L) or less marked hyponatremia that is symptomatic and has resisted correction with fluid restriction. Used for hyponatremia associated with congestive heart failure, liver cirrhosis, and syndrome of inappropriate antidiuretic hormone secretion. Initiate or reinitiate in hospital environment only.

http://emedicine.medscape.com/article/767624-treatment

Subarachnoid Hemorrhages (SAH)

What is SAH?

-bleeding in subarachnoid space

-commonly refers to nontraumatic type of hemorrhages eg: ruptures of berry aneurysm and arteriovenous malformation (AVM).

What are the signs and symptoms?

*-sudden onset of a severe headache which often worse near the back of the head.

-nausea and/or vomiting

-symptoms of meningeal irritation (eg, neck stiffness, low back pain, bilateral leg pain. Take several hours to develop.

-photophobia and visual changes

-loss of consciousness (50% of ppl at the time of bleeding onset)

-mood and personality changes

What causes SAH?

-Primary SAH may results from ruptures of: saccular aneurysm**, AVM **, mycotic aneurismal rupture, angioma, neoplasm, cortical thrombosis.

-congenital causes

-head injury

-use of blood thinners

-idiopathic

Risk factors:

-aneurysms in other blood vessels

-Fibromuscular dysplasia (FMD) and other connective tissue disorders associated with aneurysm or weakened blood vessels.

-high blood pressure

-history of polycystic kidney disease

-smoking

Physical examination:

-stiff neck due to irritation by blood of the meninges

-neurological exam may show signs of decreased nerve and brain function (

- eye exam may show decreased eye movement (sign of damage CN).

Investigation:

-head CT scan (immediately if SAH is suspected)

-lumbar puncture (SAH patients will have blood in their spinal fluid)

-CT scan angiography à evidence of aneurism

-cerebral angiography à show small aneurisms or other vascular problems

-tanscranial Doppler ultrasound à blood flow in the arteries

-MRI and magnetic resonance angiography (MRA) can be used.

How to treat SAH?

-treatment aims are to save the life, repair the cause of bleeding, relieve symptoms and prevent complications.

-surgery

References:

http://www.nlm.nih.gov/medlineplus/ency/article/000701.htm

http://emedicine.medscape.com/article/794076-overview