The mechanisms of injury that are associated with the development of SDH are a strong direct force to the

head or an acceleration-deceleration force. A subdural hematoma (American spelling) or subdural haematoma (British spelling), also known as a subdural haemorrhage (SDH), is a type of hematoma,usually associated with traumatic brain injury. Blood gathers within the outermost meningeal layer, between the dura mater, which adheres to the skull, and the arachnoid mater, which envelops the brain. Usually resulting from tears in bridging veins which cross the subdural space, subdural hemorrhages may cause an increase in intracranial pressure (ICP), which can cause compression of and damage to delicate brain tissue. Subdural hematomas are often life-threatening when acute. Chronic subdural hematomas, however, have better prognosis if properly managed. In contrast, epidural hematomas are usually caused by tears in arteries, resulting in a build-up of blood between the dura mater and skull. Classification Subdural hematomas are divided into acute, subacute, and chronic, depending on the speed of their onset.[1] Acute subdural hematomas that are due to trauma are the most lethal of all head injuries and have a high mortality rate if they are not rapidly treated with surgical decompression.[2] Acute bleeds often develop after high speed acceleration or deceleration injuries and are increasingly severe with larger hematomas. They are most severe if associated with cerebral contusions.[3] Though much faster than chronic subdural bleeds, acute subdural bleeding is usually venous and therefore slower than the usually arterial bleeding of an epidural hemorrhage. Acute subdural bleeds have a high mortality rate, higher even than epidural hematomas and diffuse brain injuries, because the force (acceleration/deceleration) required to cause them causes other severe injuries as well.[4] The mortality rate associated with acute subdural hematoma is around 60 to 80%.[5] Symptoms of subdural hemorrhage have a slower onset than those of epidural hemorrhages because the lower pressure veins bleed more slowly than arteries. Therefore, signs and symptoms may show up in minutes, if not immediately[10] but can be delayed as much as 2 weeks.[11] If the bleeds are large enough to put pressure on the brain, signs of increased ICP or damage to part of the brain will be present.[3] Other signs and symptoms of subdural hematoma can include any combination of the following:

Causes

A history of recent head injury Loss of consciousness or fluctuating levels of consciousness Irritability Seizures Pain Numbness Headache (either constant or fluctuating) Dizziness Disorientation Amnesia

Weakness or lethargy Nausea or vomiting Loss of appetite Personality changes Inability to speak or slurred speech Ataxia, or difficulty walking Altered breathing patterns Hearing loss or hearing ringing (tinnitus) Blurred Vision Deviated gaze, or abnormal movement of the eyes.[3]

Subdural hematomas are most often caused by head injury, when rapidly changing velocities within the skull may stretch and tear small bridging veins. Subdural hematomas due to head injury are described as traumatic. Much more common than epidural hemorrhages, subdural hemorrhages generally result from shearing injuries due to various rotational or linear forces.[3][8] Subdural hemorrhage is a classic finding in shaken baby syndrome, in which similar shearing forces classically cause intra- and pre-retinal hemorrhages. Subdural hematoma is also commonly seen in the elderly and in alcoholics, who have evidence of cerebral atrophy. Cerebral atrophy increases the length the bridging veins have to traverse between the two meningeal layers, hence increasing the likelihood of shearing forces causing a tear. It is also more common in patients on anticoagulants, especially aspirin and warfarin. Patients on these medications can have a subdural hematoma with a minor injury. A further cause can be a reduction in cerebal spinal fluid pressure which can create a low pressure in the dura and so cause rupture of the blood vessels Risk factors Factors increasing the risk of a subdural hematoma include very young or very old age. As the brain shrinks with age, the subdural space enlarges and the veins that traverse the space must travel over a wider distance, making them more vulnerable to tears. This and the fact that the elderly have more brittle veins make chronic subdural bleeds more common in older patients.[6] Infants, too, have larger subdural spaces and are more predisposed to subdural bleeds than are young adults.[3] For this reason, subdural hematoma is a common finding in shaken baby syndrome. In juveniles, an arachnoid cyst is a risk factor for a subdural hematoma.[12] Other risk factors for subdural bleeds include taking blood thinners (anticoagulants), long-term alcohol abuse, and dementia. Pathophysiology Micrograph of a chronic subdural hematoma, as demonstrated by thin strands of collagen and neovascularization. HPS stain. Collected blood from the subdural bleed may draw in water due to osmosis, causing it to expand, which may compress brain tissue and cause new bleeds by tearing other blood vessels.[6] The collected blood may even develop its own membrane.[13] In some subdural bleeds, the arachnoid layer of the meninges is torn, and cerebrospinal fluid (CSF) and blood both expand in the intracranial space, increasing pressure.[8] Substances that cause vasoconstriction may be released from the collected material in a subdural hematoma, causing further ischemia under the site by restricting blood flow to the brain.[9] When the brain is denied adequate blood flow, a biochemical cascade known as the ischemic cascade is unleashed, and may ultimately lead to brain cell death.

The body gradually reabsorbs the clot and replaces it with granulation tissue. Diagnosis

Subdural hematomas occur most often around the tops and sides of the frontal and parietal lobes.[3][8] They also occur in the posterior cranial fossa, and near the falx cerebri and tentorium cerebelli.[3] Unlike epidural hematomas, which cannot expand past the sutures of the skull, subdural hematomas can expand along the inside of the skull, creating a concave shape that follows the curve of the brain, stopping only at the dural reflections like the tentorium cerebelli and falx cerebri. On a CT scan, subdural hematomas are classically crescent-shaped, with a concave surface away from the skull. However, they can have a convex appearance, especially in the early stage of bleeding. This may cause difficulty in distinguishing between subdural and epidural hemorrhages. A more reliable indicator of subdural hemorrhage is its involvement of a larger portion of the cerebral hemisphere since it can cross suture lines, unlike an epidural hemorrhage. Subdural blood can also be seen as a layering density along the tentorium cerebelli. This can be a chronic, stable process, since the feeding system is low-pressure. In such cases, subtle signs of bleeding such as effacement of sulci or medial displacement of the junction between gray matter and white matter may be apparent. A chronic bleed can be the same density as brain tissue (called isodense to brain), meaning that it will show up on CT scan as the same shade as brain tissue, potentially obscuring the finding. http://en.wikipedia.org/wiki/Subdural_hematoma

Pathophysiology The usual mechanism that produces an acute subdural hematoma is a high-speed impact to the skull. This causes brain tissue to accelerate or decelerate relative to the fixed dural structures, tearing blood vessels. Often, the torn blood vessel is a vein that connects the cortical surface of the brain to a dural sinus (termed a bridging vein). In elderly persons, the bridging veins may already be stretched because of brain atrophy (shrinkage that occurs with age). Alternatively, a cortical vessel, either a vein or small artery, can be damaged by direct injury or laceration. An acute subdural hematoma due to a ruptured cortical artery may be associated with only minor head injury, possibly without an associated cerebral contusion. In one study, the ruptured cortical arteries were found to be located around the sylvian fissure.[3] The head trauma may also cause associated brain hematomas or contusions, subarachnoid hemorrhage, and diffuse axonal injury. Secondary brain injuries may include edema, infarction, secondary hemorrhage, and brain herniation. Typically, low-pressure venous bleeding from bridging veins dissects the arachnoid away from the dura, and the blood layers out along the cerebral convexity. Cerebral injury results from direct pressure, increased intracranial pressure (ICP), or associated intraparenchymal insults. In the subacute phase, the clotted blood liquefies. Occasionally, the cellular elements layer can appear on CT imaging as a hematocrit-like effect. In the chronic phase, cellular elements have disintegrated, and a collection of serous fluid remains in the subdural space. In rare cases, calcification develops. Much less common causes of subdural hematoma involve coagulopathies and ruptured intracranial aneurysms. Subdural hematomas have even been reported to be caused by intracranial tumors. It has been asserted that the primary brain injury associated with subdural hematoma plays a major role in mortality. However, most subdural hematomas are thought to result from torn bridging veins, as judged by surgery or autopsy. Furthermore, not all subdural hematomas are associated with diffuse parenchymal injury. As mentioned earlier, many patients who sustain these lesions are able to speak before their condition deterioratesan unlikely scenario in patients who sustain diffuse damage. Using a primate model, Gennarelli and Thibault demonstrated that the rate of acceleration-deceleration of the head was the major determinant of bridging vein failure. By using an apparatus that controlled head movement and minimized impact or contact phenomena, they were able to produce acute subdural hematomas in rhesus monkeys. In all cases, the sagittal movement of the head produced by an angular acceleration caused rupture of parasagittal bridging veins and an overlying subdural hematoma. Gennarelli and Thibault reported that their results were consistent with the clinical causes of subdural hematoma, in that 72% are associated with falls and assaults and only 24% are associated with vehicular trauma. The acceleration (or deceleration) rates caused by falls and assaults are greater than those caused by the energy-absorbing mechanisms in cars, such as dashboard padding, deformable steering wheels, and laminated windshields.[4] Acute subdural hematoma Investigation of brain physiological and biochemical parameters in patients with acute traumatic subdural hematoma has suggested variables that might be associated with secondary injury to the brain. In a study of brain biochemical patterns after acute subdural hematoma evacuation, Hlatky et al found that postsurgical patients who succumbed to their injury exhibited lower values of brain tissue oxygen tension and higher dialysate values of lactate and pyruvate in the brain underlying the hematoma. They suggested that identification of this brain biochemistry pattern after surgery might signify an evolving brain injury that warrants further evaluation or treatment.[5] Cerebral blood flow (CBF) can become markedly reduced. Schroder et al reported that in 2 patients with acute subdural hematoma requiring emergent craniotomy, the hemisphere ipsilateral to the subdural hematoma demonstrated lower CBF than the contralateral hemisphere. Furthermore, CBF in both hemispheres was lower than normal.[6]

Impressive increases in CBF and cerebral blood volume (CBV) that could not be attributed to pCO2 or blood pressure changes were noted immediately after surgery. The authors speculated that the decreased CBV caused by the subdural hematoma was a result of a compressed microcirculation, which was caused by increased ICP.[6] http://emedicine.medscape.com/article/1137207-overview#a0104

subdural hematoma usually occurs slowly and results from venous bleeding as a result of tearing of the vein(s). Long term alcoholism also contributes to liver problems (coagulopathy) that result in easy bleeding with any trauma. (Do you see these linkages that I'm giving you that you need for your concept map?) You need to make these pathophysiological connections in doing this care plan. A subdural hematoma is the result of an increase in the intracranial pressure in the brain. Increased intracranial pressure obstructs the absorption of cerebrospinal fluid (CSF) and affects the function of the nerve cells which can lead to brainstem compression and death. The signs and symptoms of intracellular pressure include (you will find others in the weblinks I listed for you):

slurred speech dilated, nonreactive pupils, often ipsilateral (on the same side) to the location of the hematoma (http://www.healthcare.uiowa.edu/igec...p?categoryID=8 - assessment tools for sensory perception) changes in motor function from weakness to hemiplegia with positive Bablinski's reflex (dorsiflexion of the ankle and great toes with fanning of the other toes), decorticate (flexion of one or both arms and stiff extension of the legs) or decerebrate (stiff extension of one or both arms and/or legs) posturing, flaccidity (no motor response at all in any extremity) and seizures hemiparesis (one-sided paralysis) contralateral (on the opposite side) to the hematoma balance problems and impaired gait (if the patient is able to ambulate) (http://www.healthcare.uiowa.edu/igec...p?categoryID=3 - assessment toold for gail and mobility) dizziness declining levels of consciousness from restlessness to confusion to coma o alert wakefulness o restlessness o drowsiness o confusion o delirium (http://www.healthcare.uiowa.edu/igec...p?categoryID=1 - assessment tools for dementia and delirium) o stupor o coma various levels of dementia is usually a specific finding in patients with subdural hematomas headache abnormal respirations a rise in blood pressure with widening pulse pressure slowing of the pulse an elevated temperature vomiting CSF drainage from the ears or nose

Any of these signs will lead you to nursing diagnoses of

Acute Pain Ineffective Tissue Perfusion: Cerebral Decreased Intracranial Adaptive Capacity (use this only if the patient is in ICU and ICP pressures are being measured) Risk for Infection Risk for Injury

Definition

A subdural haematoma (SDH) is a collection of clotting blood that forms in the subdural space. This may be: o An acute SDH. o A subacute SDH (this phase begins 3-7 days after the initial injury). o A chronic SDH (this phase begins 2-3 weeks after the initial injury). A simple SDH is when there is no associated parenchymal injury. A complicated SDH is when there is associated underlying parenchymal injury, such as contusion.

Pathophysiology

An acute subdural haematoma (SDH) is caused by either: o Bleeding from a damaged cortical artery. o Bleeding from an underlying parenchymal injury. o Tearing of bridging veins from the cortex to one of the draining venous sinuses.

Blunt head trauma is the usual mechanism of injury but spontaneous SDH can arise as a consequence of clotting disorder, arteriovenous malformations/aneurysms or other conditions. In the subacute phase the collection of clotted blood liquifies. In the chronic phase it becomes a collection of serous fluid in the subdural space.

At-risk groups

The elderly:

o o
Alcoholics:

Cerebral atrophy can occur in people over the age of 60, causing tension on the veins, which may also be weaker and more susceptible to injury as a consequence of age. Chronic subdural haematoma is more common in this age group.[4]

Alcohol misuse leads to a risk of thrombocytopenia, prolonged bleeding times and blunt head trauma and is a risk factor for SDH.[5] Alcoholism also causes cerebral atrophy which can put tension on the bridging veins. People on anticoagulation treatment:[6] o Anticoagulation treatment (including with aspirin or warfarin) is another risk factor.[7]

o o

Epidemiology

A subdural haematoma (SDH) can occur in about one third of people with a severe head injury.[8] It is more common with increasing age, as described above. One study found a prevalence of 7.35 cases per 100,000 population in those aged 70-79 years.[9] A UK-based epidemiological study found that the annual incidence of SDH/effusion in infants is approximately 12.5 cases per 100,000 population in 0-2 year-olds and approximately 24 cases per 100,000 in 0-1 year-olds.[10] The majority of cases were deemed to be due to non-accidental injury (57%). Other causes included: o Perinatal complications. o Meningitis. o Undetermined cause. o Accidental head injury. o Non-traumatic medical conditions. Spontaneous intracranial hypotension has also been reported as a rare cause.[11]

Presentation Acute subdural haematoma (SDH)

Usually presents shortly after a moderate-to-severe head injury. Loss of consciousness may occur but not always.[12] There may be a 'lucid interval' of a few hours after the injury where the patient appears relatively well and normal but subsequently deteriorates and loses consciousness as the haematoma forms.

http://www.patient.co.uk/doctor/Subdural-Haematoma.htm Brain and spinal cord protection is made possible by enclosing these structures within bones such as the skull and the verterbrae, presence of the CSF that creates a watery cushion and the presence of the membranes or meninges. This section will focus the discussion about the function and anatomy of the membranes or meninges. Definition The central nervous system structures are covered and protected by the three layers of meninges. Since nervous tissues are very soft and delicate even when just exposed to the slightest pressure, presence of intact meninges play a very vital role in the normal functioning of the structures of the central nervous system. Layers of Meninges Meninges are divided into three layers: 1. 2. 3. Outermost meningeal layer this is the leathery dura mater and is a double layered membrane. It is tough or hard covering that surrounds the brain. One layer of this mater is attached to the innermost surface of the skull forming the periosteum or the periosteal layer.the outermost layer, called the menigeal layer forms the outer coverings of the brain and it continues and becomes the dura mater of the spinal cord. Middle meningeal layer this is the weblike arachnoid mater. It has threadlike extensions that span the subarachenoid space to attach to the innermost membrane which is called the pia mater. Innermost meningeal layer this is called the pia mater, otherwise known as the gentle layer. Pia mater is a delicate surface that tightly attaches the surface of the brain and spinal cord.

Spaces Between the Layers:

Epidural Space Between the dura mater and the skull. Common location for hemorrhaging in the brain. Subdural Space Between the dura mater and the middle layer of the meninges, the arachnoid mater. When bleeding occurs, blood may collect here and push down on the lower layers of the meninges, possible causing brain damage. Subarachanoid Space From the fourth ventricle, the cerebrospinal fluid passes into the subarachnoid space where it circulates around the outside of the brain and spinal cord and eventually makes its way to the superior sagittal sinus via the arachnoid granulations also called arachnoid villi. In the superior sagittal sinus, the cerebrospinal fluid is reabsorbed into the blood stream. Cerebrospinal fluid (CSF) clear, saline bodily fluid that occupies the subarachnoid space and the ventricular system around and inside the brain. It is produced continuously at a steady rate and is essential for the normal functioning of the CNS. It acts as a cushion for the neuraxis, also bringing nutrients to the brain and spinal cord and removing waste from the system. Dura Mater Most superior of the layers it is tough and inflexible and forms several structures that separate the cranial cavity into compartments and protect the brain from displacement. Arachnoid Mater Middle layer of the meninges makes arachnoid villi, small protrusions through the dura mater into the venous sinuses of the brain, which allow CSF to exit the sub-arachnoid space and enter the blood stream. Cerebrospinal fluid (CSF) flows under the arachnoid in the subarachnoid space. Pia Mater, or Pia The delicate innermost layer of the meninges a thin fibrous tissue that is impermeable to fluid which allows it to enclose CSF (cerebrospinal fluid). By containing CSF, pia works with the other meningeal layers to protect and cushion the brain. Allows blood vessels to pass through and nourish the brain. The perivascular space created between blood vessels and pia mater functions as a lymphatic system for the brain. Lines the brain down into its sulci (folds). PHYSIOLOGY OF CSF FORMATION AND FLOW CSF is produced by the choroid plexus in the lateral, third, and fourth ventricles, and circulates through the subarachnoid space between the arachnoid mater and the pia mater. The choroid plexus consists of projections of vessels and pia mater that protrude into the ventricular cavities as frond-like villi containing capillaries in loose connective stroma. A specialized layer of ependymal cells called the choroidal epithelium overlies these villi (figure 1). CSF is formed in the choroid plexus by both filtration and active transport. In normal adults, the CSF volume is 125 to 150 mL; approximately 20 percent of the CSF is contained in the ventricles; the rest is contained in the subarachnoid space in the cranium and spinal cord. The normal rate of CSF production is approximately 20 mL per hour. CSF circulates from the lateral ventricles into the third ventricle and then the fourth ventricle via the cerebral aqueduct. Thereafter, CSF passes through apertures in the fourth ventricle into the subarachnoid space at the base of the brain and then flows over the convexities of the brain and down the length of the spinal cord. The CSF is propelled along the neuroaxis by a cranio-caudal pulsatile wave induced by flow in the cerebral arteries and by the associated expansions of the vascular compartment in the cranial vault. http://www.lazada.com.ph/shop-smartphones/?operating_system=Android

Subarachnoid hemorrhage is sudden bleeding into the subarachnoid space. The most common cause of spontaneous bleeding is a ruptured aneurysm. Symptoms include sudden,
severe headache, usually with loss or impairment of consciousness. Secondary vasospasm (causing focal brain ischemia), meningismus, and hydrocephalus (causing persistent headache and obtundation) are common. Diagnosis is by CT or MRI; if neuroimaging is normal, diagnosis is by CSF analysis. Treatment is with supportive measures and neurosurgery or endovascular measures, preferably in a referral center. Etiology Subarachnoid hemorrhage is bleeding between the arachnoid and pia mater. In general, head trauma is the most common cause, but traumatic subarachnoid hemorrhage is usually considered a separate disorder (see Traumatic Brain Injury (TBI)). Spontaneous (primary) subarachnoid hemorrhage usually results from ruptured aneurysms. A congenital intracranial saccular or berry aneurysm is the cause in about 85% of patients. Bleeding may stop spontaneously. Aneurysmal hemorrhage may occur at any age but is most common from age 40 to 65. Less common causes are mycotic aneurysms, arteriovenous malformations, and bleeding disorders. Pathophysiology Blood in the subarachnoid space causes a chemical meningitis that commonly increases intracranial pressure for days or a few weeks. Secondary vasospasm may cause focal brain ischemia; about 25% of patients develop signs of a transient ischemic attack (TIA) or ischemic stroke. Brain edema is maximal and risk of vasospasm and subsequent infarction (called angry brain) is highest between 72 h and 10 days. Secondary acute hydrocephalus is also common. A 2nd rupture (rebleeding) sometimes occurs, most often within about 7 days. Symptoms and Signs Headache is usually severe, peaking within seconds. Loss of consciousness may follow, usually immediately but sometimes not for several hours. Severe neurologic deficits may develop and become irreversible within minutes or a few hours. Sensorium may be impaired, and patients may become restless. Seizures are possible. Usually, the neck is not stiff initially unless the cerebellar tonsils herniate. However, within 24 h, chemical meningitis causes moderate to marked meningismus, vomiting, and sometimes bilateral extensor plantar responses. Heart or respiratory rate is often abnormal. Fever, continued headaches, and confusion are common during the first 5 to 10 days. Secondary hydrocephalus may cause headache, obtundation, and motor deficits that persist for weeks. Rebleeding may cause recurrent or new symptoms.

http://www.merckmanuals.com/professional/neurologic_disorders/stroke_cva/subarachnoid_hemorrhage_sah.html