INTRODUCTION

Cerebrovascular disease is a group of brain dysfunctions related to disease of the blood vessels supplying the brain. Hypertension is the most important cause; it damages the blood vessel lining, endothelium, exposing the underlying collagen where platelets aggregate to initiate a repairing process which is not always complete and perfect. Sustained hypertension permanently changes the architecture of the blood vessels making them narrow, stiff, deformed, uneven and more vulnerable to fluctuations in blood pressure. A fall in blood pressure during sleep can then lead to a marked reduction in blood flow in the narrowed blood vessels causing ischemic stroke in the morning. Conversely, a sudden rise in blood pressure due to excitation during the daytime can cause tearing of the blood vessels resulting in intracranial hemorrhage. Cerebrovascular disease primarily affects people who are elderly or have a history of diabetes, smoking, or ischemic heart disease. The results of cerebrovascular disease can include a stroke, or occasionally a hemorrhagic stroke. Ischemia or other blood vessel dysfunctions can affect the person during a cerebrovascular incident. Carotid artery affects retina, cerebral hemisphere, or both. Retinal: Transient blackouts; the sense of a shade pulled over the eyes. Cerebral: Contralateral (opposite sided) paralysis of a single body part; paralysis of one side of the body; localized tingling, numbness; hemianopic visual loss; aphasia (loss of speech); rare loss of consciousness. Vertebrobasilar: Bilateral visual disturbance including dim, gray, or blurred vision or temporary total blindness; diplopia (double vision). Labyrinth/medulla: Vertigo; unsteadiness; nausea; vomiting. Brainstem: Slurring dysarthria (tongue weakness causing impaired speech); dysphagia (difficulty swallowing); numbness, weakness; all four limb paresthesia; drop attacks from sudden loss of postural tone are basilar in origin; a vertebrobasilar artery occlusion episode causes symptoms to be induced by abrupt position changes. In a healthy, anatomical structure of the body, the carotid arteries form the main blood supply to the brain. Following a stroke, voluntary control of the muscles may be lost, depending on the type of stroke the victim is encountering. Strokes can also result from embolism or due to a ruptured blood vessel. Embolism blocks small arteries within the brain, causing dysfunction to occur. Spontaneous rupture of a blood vessel in the brain causes a hemorrhagic stroke. Another form of cerebrovascular disease includes aneurysms. In females with defective collagen, the weak branching points of arteries give rise to protrusions with a very thin covering of endothelium that can tear to bleed easily with minimal rise of blood pressure. This can also occur with defective capillaries caused by tissue cholesterol deposition especially in hypertensive subjects with or without dyslipidemia. If bleeding occurs in this process, the resulting effect is a hemorrhagic strokein the form of subarachnoid hemorrhage, intracerebral hemorrhage or both. In the main structure, the carotid arteries overspread the majority of the cerebrum. The common carotid artery divides into the internal and the external cartoid arteries. The internal carotid artery becomes the anterior cerebral artery and the middle central artery. The ACA transmits blood to the frontal parietal and a small part of the occipital lobe. The MCA is the largest branch of the internal

carotid artery. From the Basillar artery are two posterior cerebral arteries. Branches of the Basillar and PCA supply the occipital lobe, brain stem, and the cerebellum. Ischemia is the loss of blood flow to the focal region of the brain. The beginning process of this is quite rapid. The duration of a stroke is usually two to fifteen minutes. One side of the face, hand, or arm may swell up. During this time, the person may lose conscious control and faint. Brain deficits may improve over a maximum of 72 hours. Deficits do not resolve in all cases. The neurological recovery period includes stable, to improving, brain function. Stable is the period by which neither nutrient supply is regained, nor is it lost. Improving, depending on a hospital code, generally means that the arteries gain control and blood flow functions consistently within the brain. The carotid arteries connect to the vertebral arteries. These branch off into the cerebellar and posterior meningenial arteries, which supply the back of the brain. Also, during ischemia, interneurons weaken, causing an insufficient amount to perform vital functions to be present. The neuroglis become congested or maintain loss during a cerebrovascular accident. If impulse amount ceases, then life itself will cease and the victim may enter the stage of clinical death. Neural pathways weaken, therefore decreasing action potential. The neural arc, which in general consists of sensory and motor neurons, weaken as well. The muscles become paralyzed, in some cases for life. Paralysis also includes the weakening of the receptors in the body, unless improvement is made. Cerebrovascular damage to the brain is what makes it difficult for receptors to receive the impulse and transmit it of a neuron. This chemical reaction is then transmitted creating a poor reflex to the body. The meninges that also protect the brain and spinal cord are deeply weakened, allowing the victim to suffer vast transmission of diseases or unstable growth or maintenance if the victim is not in resting position. Infection of the brain may then lead to inflammation and conditions such as Alzheimer's Disease. During the stage of paralysis, the spinal tracts do not have much to do with the enduring condition of cerebrovascular disease, either, in time may shorten the life of a victim who is suffering because the nutrient supply is weakened in transmission during cerebrovascular disease. Descending and ascending tracts will generally be cut off during cerebrovascular disease, which conduct impulses down from the cord of the brain. This is known as anesthesia in a minor case. In a healthy body, the cerebrospinal fluid (also known as CSF) may also weaken the choroid plexus, into a network of brain capillaries. Certain types of hydrocephalus ("water" or CSF on the brain) may be treated by using a shunt (medical) or a cerebral shunt, which involves inserting a hollow tube through a blocked channel so the CSF can be used to be drained to another portion of the body. The dermatomes are a skin surface area which is regulated by the spinal cord. During a stroke, these may be damaged. Vascular dementia usually involves arterioles and capillaries rather than the larger cerebral arteries. Blockages and ruptures occur all over the brain, but most severely in the white matter. Microscopic examination may reveal various things in the brain such as coagulated blood, lipid deposits, and other debris caused by ruptured vessels. The most common forms of cerebrovascular disease are cerebral thrombosis (40% of cases) and cerebral embolism (30%), followed by cerebral hemorrhage (20%). Cerebrovascular disease is primarily one of old age; the risk for developing it goes up significantly after 65. CVD tends to occur earlier than Alzheimer's Disease (which is rare before the age of 80). In some countries such as Japan, CVD is more common than AD. CVD occurs more rarely in younger people due to conditions such as syphilis that lead to artery damage and strokes.

Atherosclerosis is one of the conditions that can cause cerebrovascular disease. During this process, high cholesterol levels coupled with inflammation in areas of the arteries in the brain can cause the cholesterol to build up in the vessel in the form of a thick, waxy plaque. This plaque can limit, or completely obstruct, blood flow to the brain, causing a stroke, transient ischemic attacks, or dementia, which may lead to a variety of other health complications. Another form of cerebrovascular disease includes aneurysms. In females with defective collagen, the weak branching points of arteries give rise to protrusions with a very thin covering of endothelium that can tear to bleed easily with minimal rise of blood pressure. This can also occur with defective capillaries caused by tissue cholesterol deposition especially in hypertensive subjects with or without dyslipidemia. If bleeding occurs in this process, the resulting effect is a hemorrhagic stroke in the form of subarachnoid hemorrhage, intracerebral hemorrhage or both. Types of cerebrovascular disease There are a number of different types of cerebrovascular disease. The four most common types are: stroke a serious medical condition where the blood supply to the brain is interrupted transient ischaemic attack (TIA) a temporary fall in the brain's blood supply, resulting in a lack of oxygen to the brain subarachnoid haemorrhage an uncommon cause of stroke where blood leaks out of the brain's blood vessels vascular dementia problems with the blood circulation, leading to parts of the brain not receiving enough blood and oxygen According to the National Stroke Association (1999), strokes more often occur abruptly, with the following symptoms which often develop suddenly: Difficulty standing or walking, dizziness, loss of balance, loss of coordination Numbness in the face, arm or leg weakness, particularly on one side of the body Confusion, difficulty speaking or understanding Vision difficulty in one or both eyes Severe headaches that have no known cause Other important, but less common stroke symptoms include: Nausea, fever, and vomiting that is different from a viral illness in the speed of onset (begins in minutes or hours instead of over several days) Carotid artery effects retina, cerebral hemisphere, or both. Retinal Transient blackouts; the sense of a shade pulled over the eyes. Cerebral Contralateral (opposite sided) paralysis of a single body part; paralysis of one side of the body; localized tingling, numbness; hemianopic visual loss; aphasia (loss of speech); rare loss of consciousness. Vertebrobasilar Bilateral visual disturbance including dim, gray, or blurred vision or temporary total blindness; diplopia (double vision). Labyrinth/medulla Vertigo; unsteadiness; nausea; vomiting. Brainstem Slurring dysarthria (tongue weakness causing impaired speech);dysphagia (difficulty swallowing); numbness, weakness; all four limb paresthesia; drop attacks from sudden loss of postural tone are basilar in origin; a vertebrobasilar artery occlusion episode causes symptoms to be induced by abrupt position changes.

Causes of Cerebrovascular Disease Ischemic stroke occurs when a blood vessel that supplies blood to the brain is blocked by a blood clot. A clot may form in an artery that is already very narrow. This is called a thrombus. If it completely blocks the artery, it is called a thrombotic stroke. Also a clot may break off from somewhere in the body and travel up to the brain to block a smaller artery. This is called an embolism. It causes an embolic stroke. Ischemic strokes may also be caused by blood clots that form in the heart. These clots travel through the blood and can get stuck in the small arteries of the brain. This is known as a cerebral embolism. Certain drugs and medical conditions can make your blood more likely to clot and raise your risk for ischemic stroke. A common cause of ischemic stroke in people under age 40 is carotid dissection, or a tear in the lining of the carotid artery. The tear lets blood flow between the layers of the carotid artery. This causes narrowing of the carotid artery that is not due to plaque buildup. Hemorrhagic stroke occurs when a blood vessel in part of the brain becomes weak and bursts open, causing blood to leak into the brain. Some people have defects in the blood vessels of the brain that make this more likely. The flow of blood that occurs after the blood vessel ruptures damages brain cells. Major modifiable risk factors include hypertension, smoking, obesity, and diabetes. Diagnosis In the physical examination, a doctor listens with the help of a stethoscope to detect abnormal sounds of blood flow (called bruit) on the neck. However, in severe cases of atherosclerosis, the bruit is less common. A physician may look for specific neurological, motor and sensory deficits such as changes in vision or visual fields, abnormal reflexes, abnormal eye movements, muscle weakness, decreased sensation and other changes. A Cerebral Angiography, Vertebral Angiogram or Carotid Angiogram is also a possibility. In this radiological diagnostic method in which a catheter (a long narrow flexible tube) is inserted into the patient's artery with the help of a needle and guided through the main vessels of the abdomen and chest until it is placed in the arteries of the neck. The whole procedure is monitored with the help of a fluoroscope. X-ray pictures are taken after injecting a contrast dye in the neck with the help of the catheter. A CAT scan is used to diagnose and detect hemorrhagic strokes, since blood, bone and brain tissue can be easily distinguished due to their difference in densities. It is important to note that damage from ischemic stroke cannot be detected by this scanning method. Treatment Blood platelet inhibitors such as Aspirin, Dipyridamole, Ticlopidine, Clopidogrel and Sulfinpyrazone are effective in reducing the risk for stroke. These drugs have been effective in treating patients with a history of stroke or patients at risk for a stroke event. Carotid Endarterectomy is a procedure in which an incision is made into the carotid artery and the plaque removed with the help of a dissecting tool thus enabling normal blood flow. Then the artery is repaired with sutures or a graft.

In Carotid Angioplasty and stenting a balloon tipped catheter is inserted into the artery and the balloon inflated to press against the plaque so as to flatten the plaque and reopen the artery. A tiny, slender metal mesh tube (stent) is fitted inside the carotid artery to improve the blood flow in the arteries blocked by plaque. The stent helps in preventing the artery from collapsing or closing up after the procedure is complete. Prevention Cerebrovascular disease can be best prevented by abiding by the following recommendations: quitting smoking, regular physical exercise, eating heart healthy diet with low fat content, maintaining healthy weight or avoiding obesity, controlling blood pressure, controlling hypertension, avoiding anger or chronic stress and lowering blood cholesterol.

PATIENT PROFILE & HISTORY

Patients name: Teojenes Mangas Age: 65y.o. Sex: M Civil status: married Birthday: 01/26/1948 Birth place: Danao City, Cebu c/c: Right sided weakness Dx: CVD Infarct Left MCA HPI: 3 days PTA, patient experienced headache and was suddenly unable to communicate. A few hours PTA, right side of patients extremities were not able to move already. PMH: Patient has a history of hypertension, smoker and an occasional drinker. Patient has no history of DM, asthma or any known allergies. FH: Patients family has no history of hypertension, DM, asthma or any known allergies.

PHYSICAL EXAMINATION
General Skin, Nails and Hair Head EENT Abdomen

GORDONS TYPOLOGY

LABORATORY EXAMINATION
BLOOD CHEMISTRY Sodium Potassium Chloride RESULT 141 3.67 99.5 NORMAL VALUE 135-145 3.5-5.5 98-107 INTERPRETATION Normal Normal Normal

CT SCAN SECTION 1. Sub-acute infarct involving the left frontotemporoparietal lobes and left basal ganglia (left MCA territory. 2. Small chronic infarcts at the left occipital lobe and the right periventricular region. 3. Atherosclerosis of the internal carotid artery. CBC WBC Hgb Hct MCV MCH RBC MCHC RDW MPV Platelet Neutrophil Lymphocyte Monocyte Eosinophil Basophil URINALYSIS Color Transparency Sp. Gravity pH Glucose Protein RBC WBC LIPID PROFILE Cholesterol Triglycerides HDL LDL RESULT 150.5 71.4 39.62 96.5 RESULT 14.35 172 0.51 92.3 30.3 5.49 339 13.5 9.8 193 84.7 7.9 6.8 0.5 0.1 RESULT Yellow Clear 1.020 6.0 +3 0-2 0-2 NORMAL VALUE 0-200 0-200 >60 <130 NORMAL VALUE 4.8-10.8 140-180 0.42-0.52 80-94 27-31 4.7-6.1 330-370 11-16 7.2-11.1 150-400 40-74 19-48 3-9 0-7 0-2 INTERPRETATION Cerebral Ischemia Normal Normal Normal Normal Normal Normal Normal Normal Normal Cerebral Ischemia Cerebral Ischemia Normal Normal Normal INTERPRETATION Normal Normal Normal Normal Renal insufficiency Normal Normal Normal INTERPRETATION Normal Normal Increased risk of heart disease Normal

PATHOPHYSIOLOGY
HOST Alcoholic HPN Age Sex Sedentary lifestyle AGENT N/A ENVIRONMENT N/A

Stenosis of left internal carotid artery Decreased cardiac output Compensatory RAAS Increased blood volume Increased preload, stroke volume and heart rate Increased myocardial Oxygen requirement Decreased cardiac output and ejection fraction Increased blood pressure Decreased tissue perfusion to the brain Infarct formation on the left middle cerebral artery Affects:

Left frontotemporoparietal lobe Sensation and movement of right side of the body

basal ganglia voluntary motor control

Brocas area Anomia

Wernickes area

According to AHA, men are more likely to die from stroke than women. Elderly are at higher risk of having stroke because of the loss of elasticity and build-up of plaques in the lumen of blood vessels. Hypertension plays a role in the development of plaques which causes decrease in the blood flow to tissues. Sedentary lifestyle contributes to the development of plaques as well. Smoking and alcohol contributes to the development also of plaques. A stroke occurs when the blood flow to an area of the brain is interrupted, resulting in some degree of permanent neurological damage. The two major categories of stroke are ischaemic (lack of blood and hence oxygen to an area of the brain) and haemorrhagic (bleeding from a burst or leaking blood vessel in the brain) stroke.

Narrowing is commonly the result of atherosclerosis the occurrence of fatty plaques lining the blood vessels. As the plaques grow in size, the blood vessel becomes narrowed and the blood flow to the area beyond is reduced. Damaged areas of an atherosclerotic plaque can cause a blood clot to form, which blocks the blood vessel a thrombotic stroke. Areas supplied by the middle cerebral artery include: The bulk of the lateral surface of the hemisphere; except for the superior inch of the frontal and parietal lobe (anterior cerebral artery), and the inferior part of the temporal lobe. Superior division supplies lateroinferior frontal lobe (location of Broca's area i.e. language expression) Inferior division supplies lateral temporal lobe (location of Wernicke's area i.e. language comprehension) Deep branches supply the basal ganglia as well as the internal capsule Occlusion of the middle cerebral artery results in Middle cerebral artery syndrome, potentially showing the following defects: Paralysis (-plegia) or weakness (-paresis) of the contralateral face and arm (faciobrachial) Sensory loss of the contralateral face and arm. Damage to the dominant hemisphere (usually the left hemisphere) results in aphasia i.e. Broca's or Wernicke's. Damage to the non-dominant hemisphere (usually the right hemisphere) results in contralateral neglect syndrome. Large MCA infarcts often have dviation conjugue, a gaze preference towards the side of the lesion, especially during the acute period. Contralateral homonymous hemianopsia is often present. The basal ganglia (or basal nuclei) are a group of nuclei of varied origin in the brains of vertebrates that act as a cohesive functional unit. They are situated at the base of the forebrain and are strongly connected with the cerebral cortex, thalamus, and other brain areas. The basal ganglia are associated with a variety of functions, including voluntary motor control, procedural learning relating to routine behaviors or "habits" such as bruxism, eye movements, cognitive, and emotional functions.

UGIB secondary to BPUD

Acute gastrointestinal bleeding is a potentially life-threatening abdominal emergency that remains a common cause of hospitalization. Upper gastrointestinal bleeding (UGIB) is defined as bleeding derived from a source proximal to the ligament of Treitz. Signs and symptoms Signs and symptoms of acute upper GI bleeding include the following: Hematemesis Melena Hematochezia Syncope Presyncope Dyspepsia Epigastric pain Heartburn Diffuse abdominal pain Dysphagia Weight loss Jaundice Diagnosis Orthostatic blood pressure Complete blood count with differential Hemoglobin level Type and crossmatch blood Basic metabolic profile, blood urea nitrogen, and coagulation profile Calcium level Gastrin level Endoscopy Chest radiography Nasogastric lavage Angiography (if bleeding persists and endoscopy fails to identify a bleeding site) Computed tomography scanning and ultrasonography may be indicated for the evaluation of the following: Liver disease with cirrhosis Cholecystitis with hemorrhage Pancreatitis with pseudocyst and hemorrhage Aortoenteric fistula Management Treatment includes the following: Secure the airway Insert bilateral, 16-gauge (minimum), upper extremity, peripheral intravenous lines Replace each milliliter of blood loss with 3 mL of crystalloid fluid

In patients with severe coexisting medical illnesses, pulmonary artery catheter insertion for monitoring hemodynamic cardiac performance Foley catheter placement for continuous evaluation of urinary output as a guide to renal perfusion Endoscopic hemostatic therapy for bleeding ulcers and varices Surgical repair of perforated viscus For high-risk peptic ulcer patients, high-dose intravenous proton pump inhibitors

Indications for surgery in patients with bleeding peptic ulcers include the following: Severe, life-threatening hemorrhage not responsive to resuscitative efforts Failure of medical therapy and endoscopic hemostasis with persistent recurrent bleeding A coexisting reason for surgery (eg, perforation, obstruction, malignancy) Prolonged bleeding, with loss of 50% or more of the patient's blood volume A second hospitalization for peptic ulcer hemorrhage Acute gastrointestinal (GI) bleeding is a potentially life-threatening abdominal emergency that remains a common cause of hospitalization. Upper gastrointestinal bleeding (UGIB) is defined as bleeding derived from a source proximal to the ligament of Treitz. The incidence of UGIB is approximately 100 cases per 100,000 population per year. Bleeding from the upper GI tract is approximately 4 times as common as bleeding from the lower GI tract and is a major cause of morbidity and mortality. Mortality rates from UGIB are 6-10% overall. The diagnosis of and therapy for nonvariceal upper gastrointestinal bleeding (UGIB) has evolved since the late 20th century from passive diagnostic esophagogastroduodenoscopy with medical therapy until surgical intervention was needed to active intervention with endoscopic techniques followed by angiographic and surgical approaches if endoscopic therapy fails. Variceal hemorrhage is not discussed in this article because the underlying mechanisms of bleeding are different and require different therapies. The underlying mechanisms of nonvariceal bleeding involve either arterial hemorrhage, such as in ulcer disease and mucosal deep tears, or low-pressure venous hemorrhage, as in telangiectasias and angioectasias. In variceal hemorrhage, the underlying pathophysiology is due to elevated portal pressure transmitted to esophageal and gastric varices and resulting in portal gastropathy. A bleeding ulcer is seen below. (See Etiology, below.) In patients with UGIB, comorbid illness, rather than actual bleeding, is the major cause of death. Comorbid illness has been noted in 50.9% of patients, with similar occurrences in males (48.7%) and females (55.4%). One or more comorbid illnesses have been noted in 98.3% of mortalities in UGIB; in 72.3% of patients, comorbid illnesses have been noted as the primary cause of death. Significant comorbidities have become more prevalent as the patient population with UGIB has become progressively older. In a retrospective chart review by Yavorski et al, 73.2% of deaths occurred in patients older than 60 years.

Rebleeding or continued bleeding is associated with increased mortality; therefore, differentiating the patient with a low probability of rebleeding and little comorbidity from the patient at high risk for rebleeding with serious comorbidities is imperative. Peptic ulcer disease (PUD) remains the most common cause of UGIB. In a literature review involving more than 10,000 patients with UGIB, PUD was responsible for 27-40% of all bleeding episodes. High-risk patient populations at risk for PUD include those with a history of alcohol abuse, chronic renal failure, and/or nonsteroidal anti-inflammatory drug (NSAID) use. Peptic ulcer disease is strongly associated with Helicobacter pylori infection. The organism causes disruption of the mucous barrier and has a direct inflammatory effect on gastric and duodenal mucosa, reducing mucosal defenses and increasing back diffusion of acid by loosening tight cellular junctions. This discrepancy may be due to the decrease in sensitivity of biopsy in patients with ulcer bleeding. Eradication of H pylori been demonstrated to reduce the risk of recurrent ulcers and, thus, recurrent ulcer hemorrhage after the initial episode. In fact, the proportion of UGIB cases caused by peptic ulcer disease has declined, a phenomenon that is believed to be due to the use of proton pump inhibitors (PPIs) and H pylori therapy. Duodenal ulcers are more common than gastric ulcers, but the incidence of bleeding is identical for both. In most cases, the bleeding is caused by the erosion of an artery in the base of the ulcer. In approximately 80% of patients, bleeding from a peptic ulcer stops spontaneously. Initial endoscopic attempts to maintain hemostasis have a high failure rate. Bleeding vessels larger than 1.5 mm in diameter are associated with an increased mortality rate due to the difficulty of producing adequate hemostasis with thermal probes. A minority of patients experience recurrent bleeding after endoscopic therapy, and these cases are usually associated with risk factors for rebleeding. These factors include age older than 60 years, the presence of shock upon admission, coagulopathy, active pulsatile bleeding, and the presence of cardiovascular disease. These circumstances are associated with a poorer prognosis and a higher mortality rate. Despite the dangers associated with a bleeding peptic ulcer, a study by Sung et al of 10,428 cases of such bleeding (in 9,375 patients) found that most patient deaths were not caused by it. Of the 577 deaths that occurred in the cohort, almost 80% resulted from other causes, including multiorgan failure, pulmonary conditions, and terminal malignancy. The authors concluded that the management of patients with peptic ulcers should focus not only on hemostasis but also on lowering the risk of multiorgan failure and cardiopulmonary death. Recurrent bleeding risk in peptic ulcers Forrest et al were the first to classify the stigmata of hemorrhage from peptic ulcers. Based on these classifications, the risk of recurrent bleeding can be predicted. The ulcers at highest risk for rebleeding are those that involve active arterial bleeding or those with a visible, protuberant, nonbleeding vessel in the base of the ulcer. The study not only correlated the incidence of rebleeding with the stigmata of recent bleeding and the endoscopic appearance of an ulcer, but also determined prognostic information regarding the need for surgery. Mortality was also correlated.

In patients with H pylori infection, the rate of recurrent bleeding is extremely low. This is why documenting the presence of H pylori and aggressively treating the infection are important. Patients who are not infected with H pylori may require a subsequent acid-lowering surgical procedure or longterm medical therapy for recurrent ulcer disease and bleeding. Ulcer-related UGIB As previously mentioned, peptic ulcer disease is strongly associated with H pylori infection. The organism causes disruption of the mucous barrier and has a direct inflammatory effect on gastric and duodenal mucosa. In cases of ulcer-associated UGIB, as the ulcer burrows deeper into the gastroduodenal mucosa, the process causes weakening and necrosis of the arterial wall, leading to the development of a pseudoaneurysm. The weakened wall ruptures, producing hemorrhage. The flow through the vessel varies with the fourth power of the radius; thus, small increases in vessel size can mean much larger amounts of blood flow and bleeding, with more severe hypotension and more complications, especially in older patients. Visible vessels usually range from 0.3-1.8 mm. Exsanguinating hemorrhage has been reported from larger vessels. The larger vessels are located deeper in the gastric and duodenal submucosa and serosa. Larger branches of the left gastric artery are found high on the lesser curvature, while the pancreatoduodenal artery and its major branches are located posteroinferiorly in the duodenal bulb. Annually, approximately 100,000 patients are admitted to US hospitals for therapy for UGIB. UGIB is a common occurrence throughout the world. In France, a report concludes that the mortality from UGIB has decreased from about 11% to 7%; however, a similar report from Greece finds no decrease in mortality. In a nationwide study from Spain, UGIB was 6 times more common than lower GI bleeding. The incidence of UGIB is 2-fold greater in males than in females, in all age groups; however, the death rate is similar in both sexes. The population with UGIB has become progressively older, with a concurrent increase in significant comorbidities that increase mortality. Mortality increases with older age (>60 y) in males and females. As previously mentioned, age older than 60 years is an independent marker for a poor outcome in upper gastrointestinal bleeding (UGIB), with the mortality rate ranging from 12-25% in this group of patients. The American Society for Gastrointestinal Endoscopy (ASGE) grouped patients with UGIB according to age and correlated age category to risk of mortality. The ASGE found a mortality rate of 3.3% for patients aged 21-31 years, a rate of 10.1% for those aged 41-50 years, and a rate of 14.4% for those aged 71-80 years. The following risk factors are associated with increased mortality, recurrent bleeding, the need for endoscopic hemostasis, or surgery: Age older than 60 years Severe comorbidity Active bleeding (eg, witnessed hematemesis, red blood per nasogastric tube, fresh blood per rectum) Hypotension Red blood cell transfusion greater than or equal to 6 units

Inpatient at time of bleed Severe coagulopathy

Patients who present in hemorrhagic shock have a mortality rate of up to 30%. The history and physical examination of the patient provide crucial information for the initial evaluation of persons presenting with a GI tract hemorrhage. History findings include weakness, dizziness, syncope associated with hematemesis (coffee ground vomitus), and melena (black stools with a rotten odor). Occasionally, a brisk UGIB manifests as hematochezia (red or maroon stools); the redder the stool, the more rapid the transit, which suggests a large upper tract hemorrhage. Laine and Shah found that 15% of patients presenting with hematochezia had an upper gastrointestinal source of bleeding identified at urgent esophagogastroduodenoscopy. Patients may have a history of dyspepsia (especially nocturnal symptoms), ulcer disease, early satiety, and NSAID or aspirin use. A history of recent aspirin ingestion suggests that the patient may have NSAID gastropathy with an enhanced bleeding diathesis from poor platelet adhesiveness. Many patients with UGIB who are taking NSAIDs present without dyspepsia but with hematemesis or melena as their first symptom, owing to the analgesic effect of the NSAID. Low-dose aspirin (81 mg) has been associated with UGIB with or without the addition of NSAID therapy. Using the lowest effective dose for both short-term and long-term users is recommended. Patients with a history of ulcers are at an especially increased risk for UGIB when placed on aspirin or NSAID therapy and should receive continuous acid suppression with a proton pump inhibitor (PPI). The patients ulcer history is also important because recurrence of ulcer disease is common, especially if he or she has not been treated for H pylori gastritis or antibiotic therapy has failed. Patients may present in a more subacute phase, with a history of dyspepsia and occult intestinal bleeding manifesting as a positive fecal occult blood test result or as iron deficiency anemia. A history of chronic alcohol use of more than 50 g/d or chronic hepatitis (B or C) increases the risk of variceal hemorrhage, gastric antral vascular ectasia (GAVE), or portal gastropathy. The finding of subcutaneous emphysema with a history of vomiting is suggestive of Boerhaave syndrome (esophageal perforation) and requires prompt consideration of surgical therapy. The presence of postural hypotension indicates more rapid and severe blood loss. A meta-analysis documented the incidence of acute UGIB symptoms as follows: Hematemesis - 40-50% Melena - 70-80% Hematochezia - 15-20% Either hematochezia or melena - 90-98% Syncope - 14.4% Presyncope - 43.2% Symptoms 30 days prior to admission - No percentage available Dyspepsia - 18% Epigastric pain - 41% Heartburn - 21%

Diffuse abdominal pain - 10% Dysphagia - 5% Weight loss - 12% Jaundice - 5.2%

The goal of the patient's physical examination is to evaluate for shock and blood loss. Patients present with an ulcer that has bled or is actively bleeding (although approximately 80% of ulcers stop bleeding). Hematemesis and melena are the most common presentations of acute UGIB, and patients may present with both symptoms. Assessing the patient for hemodynamic instability and clinical signs of poor perfusion is important early in the initial evaluation to properly triage patients with massive hemorrhage to ICU settings. Worrisome clinical signs and symptoms of hemodynamic compromise include tachycardia of more than 100 beats per minute (bpm), systolic blood pressure of less than 90 mm Hg, cool extremities, syncope, and other obvious signs of shock, such as ongoing brisk hematemesis or the occurrence of maroon or bright-red stools, which requires rapid blood transfusion. Pulse and blood pressure should be checked with the patient in supine and upright positions to note the effect of blood loss. Significant changes in vital signs with postural changes indicate an acute blood loss of approximately 20% or more. Signs of chronic liver disease should be noted, including spider angiomata, gynecomastia, increased luneals, splenomegaly, ascites, pedal edema, and asterixis. Signs of tumor are uncommon but portend a poor prognosis. Signs include a nodular liver, an abdominal mass, and enlarged and firm lymph nodes. The finding of telangiectasias may indicate the rare case of OslerWeber-Rendu syndrome.

PATHOPHYSIOLOGY