Upper gastrointestinal bleeding

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Upper gastrointestinal bleeding

Classification and external resources

Endoscopic image of a posterior wall duodenal ulcer with a clean base, which is a common cause of upper GI hemorrhage. ICD-10 ICD-9 eMedicine K92.2 578.9 med/3565

Upper gastrointestinal (GI) bleeding refers to hemorrhage in the upper gastrointestinal tract. The anatomic cut-off for upper GI bleeding is the ligament of Treitz, which connects the fourth portion of the duodenum to the diaphragm near the splenic flexure of the colon. Upper GI bleeds are considered medical emergencies, and require admission to hospital for urgent diagnosis and management. Due to advances in medications and endoscopy, upper GI hemorrhage is now usually treated without surgery.

Contents
[hide]

1 Presentation 2 Causes

3 Diagnosis

3.1 Diagnostic testing 3.2 Bayesian calculations 4.1 Refractory bleeding

4 Treatment

5 Epidemiology 6 See also 7 References 8 External links

[edit] Presentation
Patients with upper GI hemorrhage often present with hematemesis, coffee ground vomiting, melena, or hematochezia (maroon coloured stool) if the hemorrhage is severe. The presentation of bleeding depends on the amount and location of hemorrhage. Patients may also present with complications of anemia, including chest pain, syncope, fatigue and shortness of breath. The physical examination performed by the physician concentrates on the following things:

Vital signs, in order to determine the severity of bleeding and the timing of intervention Abdominal and rectal examination, in order to determine possible causes of hemorrhage Assessment for portal hypertension and stigmata of chronic liver disease in order to determine if the bleeding is from a variceal source.

Laboratory findings include anemia, coagulopathy, and an elevated BUN-to-creatinine ratio.

[edit] Causes

Gastric ulcer in antrum of stomach with overlying clot. Pathology was consistent with gastric lymphoma. A number of medications increase the risk of bleeding including NSAIDs and SSRIs. SSRIs double the rate of upper gastrointestinal bleeding.[1] There are many causes for upper GI hemorrhage. Causes are usually anatomically divided into their location in the upper gastrointestinal tract. People are usually stratified into having either variceal or non-variceal sources of upper GI hemorrhage, as the two have different treatment algorithms and prognosis. The causes for upper GI hemorrhage include the following:

Esophageal causes:

Esophageal varices Esophagitis Esophageal cancer Mallory-Weiss tear Gastric ulcer Gastric cancer Gastritis Gastric varices Gastric antral vascular ectasia Dieulafoy's lesions Duodenal ulcer Vascular malformation, including aorto-enteric fistulae. Fistulae are usually secondary to prior vascular surgery and usually occur at the proximal anastomosis at the third or fourth portion of the duodenum where it is retroperitoneal and near the aorta.[2][3][4] Hematobilia, or bleeding from the biliary tree Hemosuccus pancreaticus, or bleeding from the pancreatic duct Severe superior mesenteric artery syndrome

Esophageal ulcers

Gastric causes:

Duodenal causes:

[edit] Diagnosis
The diagnosis of upper GI bleeding is assumed when hematemesis is documented. In the absence of hematemesis, an upper source for GI bleeding is likely in the presence of at least two factors among: black stool, age < 50 years, and blood urea nitrogen/creatinine ratio 30 or more. In the absence of these findings, consider a nasogastric aspirate to determine the source of bleeding. If the aspirate is positive, an upper GI bleed is greater than 50%, but not high enough to be certain.

If the aspirate is negative, the source of a GI bleed is likely lower. The accuracy of the aspirate is improved by using the Gastroccult test.

[edit] Diagnostic testing

Whiting studied a cohort of 325 patients and found the odds ratios for the strongest predictors were: black stool, 16.6 (95% confidence interval [CI], 7.735.7); age < 50 years, 8.4 (95% CI, 3.222.1); and blood urea nitrogen/creatinine ratio 30 or more, 10.0 (95% CI, 4.025.6).[5] Seven (5%) of 151 with none of these factors had an upper GI tract bleed, versus 63 (93%) of 68 with 2 or 3 factors. Ernst found similar results.[6] The nasogastric aspirate can help determine the location of bleeding and thus direct initial diagnostic and treatment plans. Witting found that nasogastric aspirate has sensitivity 42%, specificity 91%, negative predictive value 64%, positive predictive value 92% and overall accuracy of 66% in differentiating upper GI bleeding from bleeding distal to the ligament of Treitz[1]. Thus, in this study a positive aspirate is more helpful than a negative aspirate. In a smaller study, Cuellar found a sensitivity of 79% and specificity of 55%[2], somewhat opposite results from Witting. Cuellar also studied the appearance of the aspirate and a summary of these results is available at the Evidence-Based On-Call database. Although the website lists these results as expired, they were available as of Oct, 16, 2006. These results are also available through the Wayback Archive and readers may consult the Archive if the original page is removed. Determining whether blood is in gastric contents, either vomited or aspirated specimens, is surprisingly difficult. Slide tests are based on orthotolidine (Hematest reagent tablets and BiliLabstix) or guaiac (Hemoccult and Gastroccult). Rosenthal found orthotolidine-based tests more sensitive than specific; the Hemoccult test's sensitivity reduced by the acidic environment; and the Gastroccult test be the most accurate [7] . Cuellar found the following results: Determining whether blood is in the gastric aspirate[8] Positive predictive Negative predictive Sensitivity Specificity value value (prevalence of 39%) (prevalence of 39%) 95% 82% 77% 96% 79% 55% 53% 20%

Finding Gastroccult Physician assessment

Holman used simulated gastric specimens and found the Hemoccult test to have significant problems with non-specificy and false-positive results, whereas the Gastroccult test was very accurate .[9] Holman found that by 120 seconds after the developer was applied, the Hemoccult test was positive on all control samples. In a study published regarding a new scoring system called the Glasgow-Blatchford bleeding score in Lancet on January 3, 2009, 16% of patients presenting with upper GI bleed had GBS score of "0", considered low. Among these patients there were no deaths or interventions needed and the patients were able to be effectively treated in an outpatient setting. [10] [11] Score is equal to "0" if the following are all present:
1. Hemoglobin level >12.9 g/dL (men) or >11.9 g/dL (women)

2. Systolic blood pressure >109 mm Hg 3. Pulse <100/minute

4. Blood urea nitrogen level <18.2 mg/dL 5. No melena or syncope

6. No past or present liver disease or heart failure

[edit] Bayesian calculations

The predictive values cited are based on the prevalences of upper GI bleeding in the corresponding studies. A clinical calculator can be used to generate predictive values for other prevalences.

[edit] Treatment

Endoscopic image of small gastric ulcer with visible vessel Emergency treatment for upper GI bleeds includes aggressive replacement of volume with intravenous solutions, and blood products if required. As patients with esophageal varices typically have coagulopathy, plasma products may have to be administered. Vital signs are continuously monitored. Early endoscopy is recommended, both as a diagnostic and therapeutic approach, as endoscopic treatment can be performed through the endoscope. Therapy depends on the type of lesion identified, and can include:

injection of adrenaline or other sclerotherapy electrocautery endoscopic clipping or banding of varices

Stigmata of high risk include active bleeding, oozing, visible vessels and red spots. Clots that are present on the bleeding lesion are usually removed in order to determine the underlying pathology, and to determine the risk for rebleeding.

Same ulcer seen after endoscopic clipping Pharmacotherapy includes the following:

Proton pump inhibitors (PPIs), which reduce gastric acid production and accelerate healing of certain gastric, duodenal and esophageal sources of hemorrhage. These can be administered orally or intravenously as an infusion depending on the risk of rebleeding. Octreotide is a somatostatin analog believed to shunt blood away from the splanchnic circulation. It has found to be a useful adjunct in management of both variceal and nonvariceal upper GI hemorrhage. It is the somatostatin analog most commonly used in North America. Terlipressin is a vasopressin analog most commonly used in Europe for variceal upper GI hemorrhage. Antibiotics are prescribed in upper GI bleeds associated with portal hypertension

If Helicobacter pylori is identified as a contributant to the source of hemorrhage, then therapy with antibiotics and a PPI is suggested.

[edit] Refractory bleeding

Refractory cases of upper GI hemorrhage may require:

Repeat esophagogastroduodenoscopy Anti-fibrinolytics, such as tranexamic acid Angiography to identify and possibly occlude the feeder vessel Recombinant Factor VII is sometimes used as an adjunct in refractory bleeding, but its utility has only been tested for variceal hemorrhage Balloon tamponade Surgery, to oversew or remove the area of hemorrhage

Certain causes of upper GI hemorrhage (including gastric ulcers require repeat endoscopy after the episode of bleeding to ascertain healing of the causative lesion.

[edit] Epidemiology
About 75% of patients presenting to the emergency room with GI bleeding have an upper source .[6] The diagnosis is easier when the patient has hematemesis. In the absence of hematemesis, 40% to 50% of patients in the emergency room with GI bleeding have an upper source [5] [8] [12]

[edit] See also

Lower gastrointestinal bleeding Forrest classification Rockall score

1. ^ "Are SSRIs associated with upper gastrointestinal bleeding in adults?". Global Family Doctor. http://www.globalfamilydoctor.com/search/GFDSearch.asp?itemNum=12057&ContType=HDA. 2. ^ Graber CJ et al. (2007). "A Stitch in Time A 64-year-old man with a history of coronary artery disease and peripheral vascular disease was admitted to the hospital with a several-month history of fevers, chills, and fatigue". New Engl J Med 357 (10): 102934. doi:10.1056/NEJMcps062601. PMID 17804848. http://content.nejm.org/cgi/content/full/357/10/1029. 3. ^ Sierra J, Kalangos A, Faidutti B, Christenson JT (2003). "Aorto-enteric fistula is a serious complication to aortic surgery. Modern trends in diagnosis and therapy". Cardiovascular surgery (London, England) 11 (3): 1858. doi:10.1016/S0967-2109(03)00004-8. PMID 12704326. 4. ^ Cendan JC, Thomas JB, Seeger JM (2004). "Twenty-one cases of aortoenteric fistula: lessons for the general surgeon". The American surgeon 70 (7): 5837; discussion 587. PMID 15279179. 5. ^ a b Witting MD, Magder L, Heins AE, Mattu A, Granja CA, Baumgarten M (2006). "ED predictors of upper gastrointestinal tract bleeding in patients without hematemesis". Am J Emerg Med 24 (3): 2805. doi:10.1016/j.ajem.2005.11.005. PMID 16635697. http://linkinghub.elsevier.com/retrieve/pii/S0735-6757(05)00427-4. 6. ^ a b Ernst AA, Haynes ML, Nick TG, Weiss SJ (1999). "Usefulness of the blood urea nitrogen/creatinine ratio in gastrointestinal bleeding". Am J Emerg Med 17 (1): 702. doi:10.1016/S0735-6757(99)90021-9. PMID 9928705. http://linkinghub.elsevier.com/retrieve/pii/S0735-6757(99)90021-9. 7. ^ Rosenthal P, Thompson J, Singh M (1984). "Detection of occult blood in gastric juice". J. Clin. Gastroenterol. 6 (2): 11921. doi:10.1097/00004836-198404000-00004. PMID 6715849. 8. ^ a b Cuellar RE, Gavaler JS, Alexander JA et al. (1990). "Gastrointestinal tract hemorrhage. The value of a nasogastric aspirate". Arch. Intern. Med. 150 (7): 13814. doi:10.1001/archinte.150.7.1381. PMID 2196022. 9. ^ Holman JS, Shwed JA (1992). "Influence of sucralfate on the detection of occult blood in simulated gastric fluid by two screening tests". Clin Pharm 11 (7): 6257. PMID 1617913. 10.^ Stanley AJ, Ashley D, Dalton HR, et al. (January 2009). "Outpatient management of patients with low-risk upper-gastrointestinal haemorrhage: multicentre validation and prospective evaluation". Lancet 373 (9657): 427. doi:10.1016/S0140-6736(08)61769-9. PMID 19091393. http://linkinghub.elsevier.com/retrieve/pii/S0140-6736(08)61769-9. [Risk Stratification and Outpatient Care for Upper GI Bleeding Lay summary]. 11.^ "Glasgow-Blatchford bleeding score". http://www.ganfyd.org/index.php?title=GlasgowBlatchford_score. Retrieved 2009-01-24. 12.^ Witting MD, Magder L, Heins AE, Mattu A, Granja CA, Baumgarten M (2004). "Usefulness and validity of diagnostic nasogastric aspiration in patients without hematemesis". Ann Emerg Med 43 (4): 52532. doi:10.1016/j.annemergmed.2003.09.002. PMID 15039700. http://linkinghub.elsevier.com/retrieve/pii/S0196064403009417.

[edit] References

[edit] External links

Patient.uk [show]

v d e

Digestive system Digestive disease Gastroenterology (primarily K20K93, 530579)

U Esophagitis (Candidal, Herpetiform) rupture (Boerhaave syndrome, Malloryp Weiss syndrome) UES (Zenker's diverticulum) LES (Barrett's esophagus) p EsophaguEsophageal motility disorder (Nutcracker esophagus, Achalasia, Diffuse s e esophageal spasm, Gastroesophageal reflux disease (GERD)) r Laryngopharyngeal reflux (LPR) Esophageal stricture Megaesophagus G I t r a c t Gastritis (Atrophic, Mntrier's disease, Gastroenteritis) Peptic (gastric) ulcer (Cushing ulcer, Dieulafoy's lesion) Dyspepsia Pyloric stenosis Stomach Achlorhydria Gastroparesis Gastroptosis Portal hypertensive gastropathy Gastric antral vascular ectasia Gastric dumping syndrome Gastric volvulus

L Enteritis (Duodenitis, Jejunitis, Ileitis) Peptic (duodenal) o Small intestine/ulcer (Curling's ulcer) Malabsorption: Coeliac Tropical w (duodenum/jejunum/ileumsprue Blind loop syndrome small bowel bacterial e )overgrowth syndrome Whipple's Short bowel syndrome r Steatorrhea Milroy disease bile acid malabsorption G I t r a c t : I n t e s Appendicitis Colitis (Pseudomembranous, Ulcerative, Ischemic, Microscopic, Collagenous, Lymphocytic) Large intestine Functional colonic disease (IBS, Intestinal (appendix/colon) pseudoobstruction/Ogilvie syndrome) Megacolon/Toxic megacolon Diverticulitis/Diverticulosis Enterocolitis (Necrotizing) IBD (Crohn's disease) vascular: Abdominal angina Mesenteric ischemia Large and/or smallAngiodysplasia Bowel obstruction: Ileus Intussusception Volvulus Fecal impaction Constipation Diarrhea (Infectious) Intestinal adhesions Proctitis (Radiation proctitis) Proctalgia fugax Rectal Rectum prolapse Anismus

t i n a l / e n t e r o p a t h y G I

Anal fissure/Anal fistula Anal abscess Anal dysplasia Anal canal Pruritus ani

b l e e d Upper (Hematemesis, Melena) Lower (Hematochezia) i n g / B I S A c c e s s o r y Hepatitis (Viral hepatitis, Autoimmune hepatitis, Alcoholic hepatitis) Cirrhosis (PBC) Fatty liver (NASH) vascular (Budd-Chiari syndrome, Hepatic veno-occlusive disease, Portal hypertension, Nutmeg liver) Liver Alcoholic liver disease Liver failure (Hepatic encephalopathy, Acute liver failure) Liver abscess (Pyogenic, Amoebic) Hepatorenal syndrome Peliosis hepatis Cholecystitis Gallstones/Cholecystolithiasis Cholesterolosis GallbladderRokitansky-Aschoff sinuses Postcholecystectomy syndrome Porcelain gallbladder Bile duct/Cholangitis (PSC, Secondary sclerosing cholangitis, Ascending)

Cholestasis/Mirizzi's syndrome Biliary fistula Haemobilia other biliaryGallstones/Cholelithiasis treecommon bile duct (Choledocholithiasis, Biliary dyskinesia) Sphincter of Oddi dysfunction Pancreatic Pancreatitis (Acute, Chronic, Hereditary, Pancreatic abscess) Pancreatic pseudocyst Exocrine pancreatic insufficiency Pancreatic fistula

A Diaphragmatic (Congenital) Hiatus b Inguinal (Indirect, Direct) Umbilical Femoral Obturator Spigelian Hernia d lumbar (Petit's, Grynfeltt-Lesshaft) o undefined location (Incisional Internal hernia) m i PeritoneaPeritonitis (Spontaneous bacterial peritonitis) Hemoperitoneum n lPneumoperitoneum o p e l v i c M: DIG anat(t, g, p)/phys/devp/enzy noco/cong/tumr, sysi/epon proc, drug(A2A/2B/3/4/5/6/7/14/16), blte

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Abdominal wall contusion

[Introduction]
Overview: abdominal wall contusion (contusion of abdominal wall) means the continuity of the abdominal wall soft tissue injury by the role of separation, does not completely interrupt anatomical and if the direction of injury force for the spiral form of the abdominal wall contusion contusion called abdominal twist, the damage is more severe clinical diagnosis should rule out intra-abdominal organ injury. slight abdominal wall contusion based on conservative therapy, suspected active bleeding early surgery.

[Cause]
abdominal contusion is caused by what the? (a) causes mostly blunt violence (such as stocks, stones) or heavy objects directly blow (a car accident, heavy compression, high drop impact) due. (B) the pathogenesis direct role in the external abdominal wall under the continuity of local tissue destruction, the skin, subcutaneous even in the deep tissue and lymphatic rupture tiny blood vessels, extravasation of blood and lymph, subcutaneous bleeding, swelling, heavier due to deep tissue of the small blood vessels rupture and hematoma formation.

[Symptoms]
What are the early symptoms of abdominal contusion? abdominal contusion is a traumatic injury in the light of its main features are: 1. injury swelling, subcutaneous congestion, local pain, local swelling and tenderness was due to leakage of blood and lymph, causing the formation of microcirculation. Different levels of the organization contusion caused by subcutaneous bleeding congestion have the following: if only a small hemorrhage in the skin itself, called petechiae; skin and subcutaneous bleeding is the formation of ecchymosis; amount of bleeding, distributed in layers of tissue infiltration room, and the accumulation of local and that the hematoma. If the hematoma is swelling more obvious. Pain due to local sensory nerve endings are damaged or because of the blood, lymph leakage, stimulated by increased abdominal pressure. 2. lesions around the muscle tension, normal or decreased bowel sounds. When muscle tension, pain and increased abdominal pressure increases, lean to reduce pain when supine. 3. can have serious abdominal muscle fibers tear and deep hematoma. 4. generally hurt more without systemic manifestations, extensive contusion, the patient may develop fever. signs according to the local site of injury to the abdominal wall contusion simple diagnosis is not difficult. However, in pediatric patients than adults because of weak abdominal muscles, it is difficult to resist external forces against a common cause of abdominal visceral injury. Therefore, for abdominal contusion, the key is timely to determine whether abdominal visceral injury and damage to other parts of the merger, so as not to delay treatment of serious consequences.

[Diet]
abdominal contusion ate? an abdominal wall contusion eat what does a body good? 1, nutrition, eat a high protein and vitamin content diet, to eat chicken, lean meat, shrimp, milk, tofu, beans and so on. 2, prevention of infection to eat needle fish, catfish, shad, day lily flowers, vegetables, taro, green bean, red bean, Malan top.

[Prevention]
abdominal contusion should be how to prevent? abdominal contusion Note: contusion to the patients immediately after bed rest, early local cooling to reduce bleeding and oozing , 48h after the heat, promote absorption of hematoma. Massage can also use milk, heparin (Hirudoid) Massage partial erasure of drugs to relieve pain, promote absorption of swelling dissipate. If the swelling is still not subside should be rushed to a hospital for treatment.

[Treatment]
abdominal contusion before treatment considerations? prevention: prevention of blunt violence (such as stocks, stones) or heavy direct attack (car accident, heavy compression, high drop impact) damage. abdominal contusion Chinese medicine treatment methods No information

abdominal contusion Western treatment surgery abdominal wall contusion main conservative treatment. The patient bed rest, early local cooling to reduce bleeding and oozing, 48h after the heat, promote absorption of hematoma. Massage can also use milk, heparin (Hirudoid) Massage partial erasure of drugs to relieve pain, promote absorption of swelling dissipate. When a large hematoma puncture and blood pressure bandage. If you still have active bleeding, the hematoma was increased, as soon as possible surgery to remove the hematoma, ligation of the bleeding point. contusion heavier, for the prevention of infection may be appropriate antibiotic therapy.

[Check]
abdominal contusion should be how? suspected of having deep organ damage or hematoma, the possible imaging, appropriate selection of B-, X-ray or CT scan.

[Confused]
abdominal contusion diseases easily confused? be differentiated with intra-abdominal organ injury. Muscle tension and tenderness is the most important intraabdominal organ injury signs, do abdominal contraction action (such as sit), and its little pain and abdominal contraction, the condition was progressively increased. The abdominal wall contusion were quiet rest and pain relief, pain when doing abdominal muscle contraction significantly increased action.

[Similar diseases]
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Diaphragmatic rupture
From Wikipedia, the free encyclopedia

Jump to: navigation, search

Diaphragmatic rupture
Classification and external resources

An X-ray showing the spleen in the left lower portion of the chest cavity (X and arrow) after a diaphragmatic tear[1] ICD-10 ICD-9 ICD-O: eMedicine S27.8 862.1 S27.8 med/3487 emerg/136

Diaphragmatic rupture (also called diaphragmatic injury or tear) is a tear of the diaphragm, the muscle across the bottom of the ribcage that plays a crucial role in respiration. Most commonly, acquired diaphragmatic tears result from physical trauma. Diaphragmatic rupture can result from blunt or penetrating trauma[2] and occurs in about 5% of cases of severe blunt trauma to the trunk.[3] Diagnostic techniques include X-ray, computed tomography, and surgical techniques such as laparotomy. Diagnosis is often difficult because signs may not show up on X-ray, or signs that do show up appear similar to other conditions. Signs and symptoms included chest and abdominal pain, difficulty breathing, and decreased lung sounds. When a tear is discovered, surgery is needed to repair it. Injuries to the diaphragm are usually accompanied by other injuries, and they indicate that more severe injury may have occurred. The outcome often depends more on associated injuries than on the diaphragmatic injury itself.[4] Since the pressure is higher in the abdominal cavity than the chest cavity, rupture of the diaphragm is almost always associated with herniation of abdominal

organs into the chest cavity, called traumatic diaphragmatic hernia.[5] This herniation can interfere with breathing, and blood supply can be cut off to organs that herniate through the diaphragm, damaging them.

Contents
[hide]

1 Signs and symptoms 2 Causes 3 Mechanism 4 Diagnosis

4.1 Location

5 Treatment 6 Prognosis

6.1 Complications

7 Epidemiology 8 History 9 References

[edit] Signs and symptoms

Breath sounds on the side of the rupture may be diminished, respiratory distress may be present, and the chest or abdomen may be painful.[3] Orthopnea, dyspnea which occurs when lying flat, may also occur,[6] and coughing is another sign.[5] In people with herniation of abdominal organs, signs of intestinal blockage or sepsis in the abdomen may be present.[5] Bowel sounds may be heard in the chest, and shoulder or epigastric pain may be present.[4] When the injury is not noticed right away, the main symptoms are those that indicate bowel obstruction.[4]

[edit] Causes
The injury may be caused by blunt trauma, penetrating trauma, and by iatrogenic causes (as a result of medical intervention), for example during surgery to the abdomen or chest.[4] Injury to the diaphragm is reported to be present in 8% of cases of blunt chest trauma.[7] In cases of blunt trauma, vehicle accidents and falls are the most common causes.[4] Penetrating trauma has been reported to cause 12.320% of cases, but it has also been proposed as a more common cause than blunt trauma; discrepancies could be due to varying regional, social, and economic factors in the areas studied.[2] Stab and gunshot wounds can cause diaphragmatic injuries.[4] Clinicians are trained to suspect diaphragmatic rupture particularly if penetrating trauma has occurred to the lower chest or upper abdomen.[8] With penetrating trauma, the contents of the abdomen may not herniate into the chest cavity right away, but they may do so later, causing the presentation to be delayed.[4] Since the diaphragm moves up and down during breathing, penetrating trauma to various parts of the torso may injure the diaphragm; penetrating injuries as high as the third rib and as low as the twelfth have been found to injure the diaphragm.[9]

[edit] Mechanism
Although the mechanism is unknown, it is proposed that a blow to the abdomen may raise the pressure within the abdomen so high that the diaphragm bursts.[4] Blunt trauma creates a large pressure gradient between the abdominal and thoracic cavities; this gradient, in addition to causing the rupture, can also cause abdominal contents to herniate into the thoracic cavity.[6] Abdominal contents in the pleural space interfere with breathing and cardiac activity.[6] They can interfere with the return of blood to the heart and prevent the heart from filling effectively, reducing cardiac output.[6] If ventilation of the lung on the side of the tear is severely inhibited, hypoxemia (low blood oxygen) results.[6] Usually the rupture is on the same side as an impact.[9] A blow to the side is three times more likely to cause diaphragmatic rupture than a blow to the front.[9]

[edit] Diagnosis
Initially, diagnosis can be difficult, especially when other severe injuries are present; thus the condition is commonly diagnosed late.[3] Chest X-ray is known to be unreliable in diagnosing diaphragmatic rupture;[6] it has low sensitivity and specificity for the injury.[5] Often another injury such as pulmonary contusion masks the injury on the X-ray film.[4] Half the time, initial Xrays are normal; in most of those that are not, hemothorax or pneumothorax is present.[6] However, there are signs detectable on X-ray films that indicate the injury. On an X-ray, the diaphragm may appear higher than normal.[3] Gas bubbles may appear in the chest, and the mediastinum may appear shifted to the side.[3] A nasogastric tube from the stomach may appear on the film in the chest cavity; this sign is pathognomonic for diaphragmatic rupture, but it is rare.[6] A contrast medium that shows up on X-ray can be inserted through the nasogastric tube to make a diagnosis.[3] The X-ray is better able to detect the injury when taken from the back with the patient upright, but this is not usually possible because the patient is usually not stable enough; thus it is usually taken from the front with the patient lying supine.[5] Positive pressure ventilation helps keep the abdominal organs from herniating into the chest cavity, but this also can prevent the injury from being discovered on an X-ray.[6] Computed tomography has an increased accuracy of diagnosis over X-ray,[7] but no specific findings on a CT scan exist to establish a diagnosis.[8] Although CT scanning increases chances that diaphragmatic rupture will be diagnosed before surgery, the rate of diagnosis before surgery is still only 3143.5%.[7] Another diagnostic method is laparotomy, but this misses diaphragmatic ruptures up to 15% of the time.[6] Often diaphragmatic injury is discovered during a laparotomy that was undertaken because of another abdominal injury.[6] Thoracoscopy is more reliable in detecting diaphragmatic tears than laparotomy and is especially useful when chronic diaphragmatic hernia is suspected.[6]

[edit] Location
Between 50 and 80% of diaphragmatic ruptures occur on the left side.[5] It is possible that the liver, which is situated in the right upper quadrant of the abdomen, cushions the diaphragm.[4] However, injuries occurring on the left side are also easier to detect in X-ray films.[6] Half of diaphragmatic ruptures that occur on the right side are associated with liver injury.[5] Injuries occurring on the right are associated with a higher rate of death and more numerous and serious accompanying injuries.[9] Bilateral diaphragmatic rupture, which occurs in 12% of ruptures, is associated with a much higher death rate (mortality) than injury that occurs on just one side.[5]

[edit] Treatment

Since the diaphragm is in constant motion with respiration, and because it is under tension, lacerations will not heal on their own.[9] Surgery is needed to repair a torn diaphragm.[3] Most of the time, the injury is repaired during laparotomy.[8] Other injuries, such as hemothorax, may present a more immediate threat and may need to be treated first if they accompany diaphragmatic rupture.[4] Video-assisted thoracoscopy may be used.[6]

[edit] Prognosis
In most cases, isolated diaphragmatic rupture is associated with good outcome if it is surgically repaired.[4] The death rate (mortality) for diaphragmatic rupture after blunt and penetrating trauma is estimated to be 1540% and 1030% respectively, but other injuries play a large role in determining outcome.[4]

[edit] Complications
A significant complication of diaphragmatic rupture is traumatic diaphragmatic herniation: organs such as the stomach that herniate into the chest cavity and may be strangulated, losing their blood supply.[3] Herniation of abdominal organs is present in 34% of people with abdominal trauma who present to a trauma center.[8]

[edit] Epidemiology
Diaphragmatic injuries are present in 17% of people with significant blunt trauma[4] and an average of 3% of abdominal injuries.[8] A high body mass index may be associated with a higher risk of diaphragmatic rupture in people involved in vehicle accidents.[4] It is rare for the diaphragm alone to be injured, especially in blunt trauma; other injuries are associated in as many as 80100% of cases.[6][7] In fact, if the diaphragm is injured, it is an indication that more severe injuries to organs may have occurred.[7] Thus, the mortality after a diagnosis of diaphragmatic rupture is 17%, with most deaths due to lung complications.[7] Common associated injuries include head injury, injuries to the aorta, fractures of the pelvis and long bones, and lacerations of the liver and spleen.[6] Associated injuries occur in over three quarters of cases.[9]

[edit] History

Ambroise Par In 1579, Ambroise Par made the first description of diaphragmatic rupture, in a French artillery captain who had been shot eight months before his death from complications of the rupture.[8] Using autopsies, Par also described diaphragmatic rupture in people who had suffered blunt and penetrating trauma.[8] Reports of diaphragmatic herniation due to injury date back at least as far as the 17th century.[8] Petit was the first to establish the difference between acquired and congenital diaphragmatic hernia, which results from a congenital malformation of the diaphragm. In 1888, Naumann repaired a hernia of the stomach into the left chest that was caused by trauma.[8]

[edit] References
1. ^ Hariharan D, Singhal R, Kinra S, Chilton A (2006). "Post traumatic intra thoracic spleen presenting with upper GI bleed! A case report". BMC Gastroenterol 6: 38. doi:10.1186/1471230X-6-38. PMC 1687187. PMID 17132174. http://www.biomedcentral.com/1471-230X/6/38. 2. ^ a b Sliker CW (March 2006). "Imaging of diaphragm injuries". Radiol Clin North Am 44 (2): 199211, vii. doi:10.1016/j.rcl.2005.10.003. PMID 16500203. 3. ^ a b c d e f g h Nolan JP (2002). "Major trauma". In Adams AP, Cashman JN, Grounds RM. Recent Advances in Anaesthesia and Intensive Care: Volume 22. London: Greenwich Medical Media. pp. 182. ISBN 1-84110-117-6. 4. ^ a b c d e f g h i j k l m n o Scharff JR, Naunheim KS (February 2007). "Traumatic diaphragmatic injuries". Thorac Surg Clin 17 (1): 815. doi:10.1016/j.thorsurg.2007.03.006. PMID 17650700. 5. ^ a b c d e f g h McGillicuddy D, Rosen P (August 2007). "Diagnostic dilemmas and current controversies in blunt chest trauma". Emerg Med Clin North Am 25 (3): 695711, viiiix. doi:10.1016/j.emc.2007.06.004. PMID 17826213. 6. ^ a b c d e f g h i j k l m n o p Karmy-Jones R, Jurkovich GJ (March 2004). "Blunt chest trauma". Current Problems in Surgery 41 (3): 211380. doi:10.1016/j.cpsurg.2003.12.004. PMID 15097979. "A sudden increase in the pressure gradient between the pleural and peritoneal cavities that occurs with high-speed blunt trauma will lead to disruptions of the diaphragm... This same pleuroperitoneal pressure gradient will also promote migration of intraperitoneal structures into the pleural space after disruption has occurred. Once the viscera have been displaced into the pleural space, both cardiovascular and respiratory functions are compromised." 7. ^ a b c d e f Weyant MJ, Fullerton DA (2008). "Blunt thoracic trauma". Seminars in Thoracic and Cardiovascular Surgery 20 (1): 2630. doi:10.1053/j.semtcvs.2008.01.002. PMID 18420123. 8. ^ a b c d e f g h i Asensio JA, Petrone P, Demitriades D, commentary by Davis JW (2003). "Injury to the diaphragm". In Moore EE, Feliciano DV, Mattox KL. Trauma. Fifth Edition. McGraw-Hill Professional. pp. 613616. ISBN 0071370692. 9. ^ a b c d e f Fleisher GR, Ludwig S, Henretig FM, Ruddy RM, Silverman BK, ed (2006). "Thoracic trauma". Textbook of Pediatric Emergency Medicine. Hagerstown, MD: Lippincott Williams & Wilkins. pp. 14467. ISBN 0-7817-5074-1.

[hide]

v d e

Chest trauma, excluding fractures (S20S29, 860862)

Cardiac and vascular: Traumatic aortic rupture (Thoracic aorta injury) circulatory system heart: Myocardial contusion/Commotio cordis Cardiac tamponade injuries Hemopericardium Myocardial rupture Lung and Pneumothorax Hemothorax Hemopneumothorax Pulmonary lower respiratory contusion Pulmonary laceration Tracheobronchial injury tract injuries Diaphragmatic rupture (Diaphragmatic hernia) M: anat(a:h/u/t/a/l,v:h/u/t/a/l)/phys/devp/cell/p noco/syva/cong/lyvd/tum proc, VA rot r, sysi/epon, injr drug(C2s+n/3/4/5/7/8/ S 9) M: HRT anat/phys/devp noco/cong/tumr, sysi/epon, injr proc, drug (C1A/1B/1C/1D), blte

M: RES

anat(n, x, l, c)/phys/devp

noco(c, p)/cong/tumr, proc, drug(R1/2/3/5/6/7) sysi/epon, injr

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Splenic trauma

Splenic injury can be either accidental or iatrogenic Most commonly associated with blunt trauma Often occurs in the presence of lower rib fractures May be common clinically apparent either early or delayed Delayed injury is usually due to rupture of subcapsular haematoma 20% of splenic injuries occur inadvertently during other abdominal operations In some patients spontaneous rupture can occur following trivial trauma Spleen is invariably abnormal due to, for example, malaria or infectious mononucleosis Clinical features depend on:

Clinical feature

Degree of hypovolaemia Presence of associated injuries

Clinical features range from left upper quadrant pain to shock and peritonitis 30 to 60% of patients have other assocaited intraperitoneal injuries

Grading
Grade 1 Minor subcapsular tear or haematoma Grade 2 Parenchymal injury not extending to the hilum Grade 3 Major parenchymal injury involving vessels and hilum Grade 4 Shattered spleen

Management

If cardiovascularly unstable requires resuscitation and early surgery If cardiovascularly stable consider either ultrasound or CT scan

If isolated Grade 1 or 2 splenic injury may be suitable for conservative management

Surgical options
Surgical management can involve either splenectomy or splenic repair Main benefit of retaining the spleen is the prevention of OPSI If splenic conservation attempted need to preserve more than 20% of tissue

Conservative management
Overall 20-40% of patients are suitable for conservative management Children can often be managed conservatively as they have Increased proportion of low grade injuries Fewer multiple injuries

Should be monitored in high dependency unit Require cardiovascular and haematological monitoring If successful patients should remain on: Bed rest for 72 hours Limited physical activity for 6 weeks

No contact sports for 6 months

Surgery needed if clinically hypovolaemic of they have a falling haematocrit Approximately 30% of patients fail conservative management Usually occurs within the first 72 hours of injury Failed conservative management often results in splenectomy Overall more spleens can often be conserved by early surgery

Picture provided by Luis Pinheiro, Hospital Saint Teotonio, Viseu, Portugal

Bibliography
Brasel K J, DeLisle C M, Olson C J, Bergstrom D C. Splenic injury: trends in evaluation and management. J Trauma 1998; 44: 283-286. Dupuy D E, Raptopoulos V, Fink M P. Current concepts in splenic trauma. J Intensive Care Med 1995; 10: 76-90. Pachter H L, Guth A A, Hefstetter S R, Spencer F C. Changing patterns in the management of splenic trauma: the impact of non-operative management. Ann Surg 1998; 227: 708-719. Sander M N, Civil I. Adult splenic injuries: treatment patterns and predictive indicators. Aust NZ J Surg 1999; 69: 430-432.

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Vomiting
Submitted by admin on Fri, 06/03/2011 - 02:06 Childhood Illnesses

Your normally happy and playful two-year-old has not been himself all day. He's been clingy, fussy, and has refused to eat his favorite foods. Then out of nowhere, he throws up what you think was breakfast. It doesn't stop there. For the next three hours he throws up every 10 minutes. This is replaced by dry- heaving until he finally falls asleep, exhausted. You are naturally worried. Here are some guidelines that will get you through the night. NOTE: Vomiting in an infant 2 months or younger is very different than older infants and children. Click here if your baby is less than 2-months-old. TOP SIX CAUSES OF VOMITING 1. Stomach flu by far the most common cause. 2. Food poisoning relax, this doesn't really mean "poison", it simply means there were some bad bacteria in the food your child ate. 3. Other intestinal illnesses there are a variety of other viral and bacterial intestinal illnesses besides the flu that can cause vomiting. Most are not serious. 4. Severe cough and cold children can often vomit after a big coughing fit. This isn't really considered a vomiting problem but rather a coughing problem. Click on Coughs, Colds & Sinus Infections for more info. 5. Bladder infection if your child has had a high fever for several days with occasional vomiting, and the urine burns or smells foul, consider this cause. 6. Intestinal obstruction now DON'T PANIC. This is by far the least common cause, but it is also the most serious and is considered a surgical emergency. See below. HOW TO DETERMINE THE CAUSE The top four causes are very difficult to distinguish at the onset because they all start out the same profuse vomiting every 5 to 30 minutes for the first 1 to 12 hours. Understanding the various causes and expected course of these three will help you determine the cause. 1. Stomach flu this is a virus that causes sudden onset of vomiting, high fever and stomach pain. Diarrhea usually begins during the first or second day. The length of vomiting varies from the "12 hour flu" to the dreaded "72 hour flu". There is no blood or stool test to diagnose this. 2. Food poisoning this is caused by bad bacteria that is present in spoiled food. The onset usually comes 2 to 12 hours after eating the food. Common food sources are: spoiled mayonnaise, chicken, fish, beef, or salad dressing. Some clues that it may be food poisoning are:
Often there is no fever Usually occurs within a few hours after eating an identifiable source of bad food such as a questionable restaurant or a picnic. Vomiting usually does not last more than 12 hours.

Therefore, if there is a high fever, you can't think of any bad food your child ate, and the vomiting lasts beyond 12 hours, it probably is not food poisoning. Diarrhea may or may not develop.

3. Other intestinal viruses or bacterial illnesses there are a variety of these. Some examples include Rotavirus, Salmonella, and E-Coli. The initial vomiting pattern, stomach pain and fever of these illnesses is the same as the stomach flu and therefore difficult to distinguish from the flu. However, in the initial period of vomiting, it is not really necessary to determine which of all these illnesses is causing it. Instead, you simply need to know how to handle the vomiting. 4. Intestinal obstruction this occurs when the intestines become twisted and is considered a medical emergency that demands immediate medical attention. The key symptom here is actually SEVERE abdominal pain. If there is only moderate or no pain, it's probably not an obstruction. Here are the symptoms:
Sudden onset of abdominal pain Persistent dark-green vomiting (bile), not just light-green mucus Usually, but not always, projectile Agonizing pain that may be constant, but may also come and go No bowel movements Pale and sweaty skin Child is overall worsening rather than staying the same or improving

GETTING THROUGH THE NIGHT The first thing to remember is DON'T PANIC. Vomiting is usually not dangerous and only rarely results in significant dehydration. Keep in mind it usually takes at least 12 hours of severe vomiting to make a child significantly dehydrated. These guidelines should help you get your child through the vomiting stage of his illness:
First stage severe vomiting every 5 30 minutes. During this time, do not attempt to give your child any food or liquids at all because they will just come right back up. This is called total bowel rest. Let the worst of the vomiting pass. If your child asks to nurse or drink something, then just offer small sips at a time, and don't expect him to keep it down.

Second stage the vomiting has started to slow down to every one or two hours. Go ahead and offer your child small sips of liquids every 5 or 10 minutes. Here are the three best liquids to try: Oral electrolyte solution such as Pedialyte has the best balance of salt, sugar, and other electrolytes Frozen popsickle or slushy made from an electrolyte solution Breastmilk is excellent for the nursing baby

A few other suggestions until you can get an electrolyte solution:

White grape juice or slushy slightly diluted with water.

Gatorade or similar drink Again, these are not as ideal, and should be replaced with Pedialyte when possible. Liquids NOT to give apple, pear, and cherry juice may have too much sugar. This can worsen diarrhea and dehydration.

Third stage vomiting is now only 2 4 times a day or stopped altogether. It is now okay to try some foods. Bland foods such as crackers, toast, soup broth, etc. Continue breastfeeding. Restart formula if formula feeding. You can mix half formula and half Pedialyte at first. This may be more easily tolerated. Continue liquids as described above.

Don't be alarmed if your child throws up this food. It may be too soon to start feeding again. Just take a step back to the second stage until the vomiting calms down again. RECTAL ACETAMINOPHEN if your child has a fever but can't keep down any medicine, we suggest acetaminophen suppositories. Click on it. ANTI-NAUSEA MEDICATION there are suppositories that can be prescribed by your doctor for kids two and older that can suppress the vomiting to get your child through the worst of it. These medications should only be used when absolutely needed. A commonly used brand is Phenergan.

WHEN NOT TO WORRY

Persistent vomiting if the vomiting seems like it's going on forever, you need to assess your child for dehydration. If he is only mildly or maybe moderately dehydrated, this generally can wait until morning to contact your doctor. Dehydration keep in mind most kids will become mildly dehydrated during a vomiting illness. Mild dehydration is not serious and often does not warrant an urgent call to your doctor. Click on it for more info on how to assess the degree of dehydration and when to call your doctor. Vomiting comes back what commonly happens is a child will get better for a day or two, and then begin vomiting again. This is generally okay. Assess which stage he seems to be in and treat it accordingly. Fever it is normal to have even high fevers for several days. Click on fever for guidelines and treatment. Blood in vomitus you may see bloody streaks in your child's vomitus. Tiny tears in the throat cause this from the pressure of vomiting. It is generally not dangerous and should pass. See below.

WHEN TO WORRY Here are some guidelines on when to call your doctor or go to the ER:

Persistent vomiting you should call your doctor if stage one vomiting continues past 8 hours in children under one, 12 hours in children one through three years old, and 16 hours in kids four and older. Large amount of blood in vomitus if the tears in the throat become too large from severe, high pressure vomiting, they can bleed significantly. If you think this is really happening, go to an emergency room promptly. This is very rare though, as the tears generally stay very tiny and only bleed slightly. Moderate to severe dehydration click here for more guidelines, but this generally warrants a call to your doctor. Meningitis a brief word here. Although vomiting is not the main sign of meningitis, it is one of them. If your child has severe headache, stiffness or pain in the BACK of the neck, high fever, and vomiting, call your doctor right away. Kidney infection again, vomiting isn't the main symptom for this, but if your child has high fevers, vomiting, and is complaining of burning with urination or the urine smells foul, you should call your doctor.

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Article Link: http://www.webmd.com/digestive-disorders/digestive-diseases-nauseavomiting WebMD Home Digestive Disorders Health Center Email a Friend Save Print Article Digestive Disorders Health Center Tools & Resources Eating for Digestive Health Are Probiotics Worthwhile? Digestive Myths From Gum to Gas What's Your Medication IQ? Diarrhea: Foods to Avoid 16 Tips for Good Digestion

Font size: AAA Share this: Nausea and Vomiting Nausea is an uneasiness of the stomach that often precedes vomiting. Vomiting is the forcible voluntary or involuntary emptying ("throwing up") of stomach contents through the mouth. What Causes Nausea or Vomiting? Nausea and vomiting are not diseases, but they are symptoms of many conditions such as: Motion sickness or seasickness Early stages of pregnancy (nausea occurs in approximately 50%-90% of all pregnancies; vomiting in 25%-55%) Medication induced vomiting Intense pain Emotional stress (fear) Gallbladder disease Food poisoning Infections (such as the "stomach flu") Overeating A reaction to certain smells or odors Heart attack Concussion or brain injury Brain tumor Ulcers Some forms of cancer Bulimia or other psychological illnesses Gastroparesis (a condition often seen in people with diabetes)

The causes of vomiting differ according to age. For children, it is common for vomiting to occur from a viral infection, food poisoning, milk allergy, motion sickness, overeating or feeding, coughing, or blocked intestines and illnesses in which the child has a high fever. The timing of the nausea or vomiting can indicate the cause. When appearing shortly after a meal, nausea or vomiting may be caused by food poisoning, gastritis (inflammation of the stomach lining), an ulcer, or bulimia. Nausea or vomiting one to eight hours after a meal may also indicate food poisoning. However, certain food borne bacteria, such as salmonella, can take longer to produce symptoms. Is Vomiting Harmful? Usually vomiting is harmless, but it can be a sign of a more serious illness. Some examples of serious conditions that may result in nausea or vomiting include concussions, meningitis (infection of the membrane linings of the brain), intestinal blockage, appendicitis, and brain tumors. Another concern is dehydration. Adults have a lower risk of becoming dehydrated because they can usually detect the symptoms of dehydration (such as increased thirst and dry lips or mouth). But, children have a greater risk of becoming dehydrated, especially if they also have diarrhea, because young children are often unable to communicate symptoms of dehydration. Adults caring for sick children need to be aware of these visible signs of dehydration: dry lips and mouth, sunken eyes, and rapid breathing or pulse. In infants, also watch for decreased urination and a sunken fontanelle (soft spot on top of the baby's head). Recurrent vomiting in pregnancy can lead to a serious condition called hyperemesis gravidarum where the mother may develop fluid and mineral imbalances that can endanger her life or that of her unborn child. When to Call the Doctor About Nausea and Vomiting Call a doctor about nausea and vomiting: If the nausea lasts for more than a few days or if there is a possibility of being pregnant. If home treatment is not working, dehydration is present, or a known injury has occurred (such as head injury or infection) that may be causing the vomiting. Adults should consult a doctor if vomiting occurs for more than one day, diarrhea and vomiting last more than 24 hours, or there are signs of moderate dehydration. Take your infant or child under six years to the doctor if vomiting lasts more than a few hours, diarrhea is present, signs of dehydration occur, there is a fever higher than 100 degrees Fahrenheit, or if the child hasn't urinated for six hours.

Take your child over age six years to the doctor if vomiting lasts one day, diarrhea combined with vomiting lasts for more than 24 hours, there are signs of dehydration, there is a fever higher than 102 degrees Fahrenheit or the child hasn't urinated for six hours. You should seek immediate medical care if any of the following situations occur with vomiting: There is blood in the vomit (bright red or "coffee grounds" in appearance) Severe headache or stiff neck Lethargy, confusion, or a decreased alertness Severe abdominal pain Fever over 101 degrees Fahrenheit Diarrhea Rapid breathing or pulse Further Reading: Gastroenteritis Treatment Gastroenteritis Gastroenteritis, Eosinophilic Slideshow: Pictures of nausea & vomiting remedies The Truth About Stomach Flu Gastroenteritis in Adults and Older Children-Related Information Gastroenteritis in Adults and Older Children-Topic Overview See All Gastroenteritis Topics Also Recommended: Is There a Product That Will Increase Fiber but Not Gas? Newly Diagnosed With Crohn's? Steps to Take Diarrhea: Three Types & Their Causes Abdominal Pain: What Could Be Causing It Foods That Can Be Problematic as You Age

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Font size: AAA Share this: Nausea and Vomiting (continued) How Is Vomiting Treated? Treatment for vomiting (regardless of age or cause) includes: Drinking gradually larger amounts of clear liquids. Avoiding solid food until the vomiting episode has passed. Temporarily discontinuing all oral medications (which can irritate the stomach and make vomiting worse). But, do not discontinue any medication before checking with your doctor first. If vomiting and diarrhea last more than 24 hours, an oral rehydrating solution such as Pedialyte should be used to prevent and treat dehydration. Pregnant women experiencing morning sickness can eat some crackers before getting out of bed or eat a high protein snack before going to bed (lean meat or cheese). Vomiting associated with cancer treatments can often be treated with another type of drug therapy. There are also prescription and nonprescription drugs that can be used to control vomiting associated with pregnancy, motion sickness and some forms of dizziness. However, consult with your doctor before using these treatments. How Can I Prevent Nausea?

There are several ways to try and prevent nausea from developing: Eat small meals throughout the day instead of three large meals. Eat slowly. Avoid hard-to-digest foods. Consume foods that are cold or room temperature to avoid nausea from the smell of hot or warm foods. Rest after eating with your head elevated about 12 inches above your feet. Drink liquids between meals instead of during meals and drink at least six to eight 8-ounce glasses of water a day to prevent dehydration (unless fluid restricted for another medical condition). Try to eat when you feel less nauseated. How Do I Prevent Vomiting Once I Feel Nauseated? When you begin to feel nauseated, you may be able to prevent vomiting by: Drink small amounts of clear, sweetened liquids such as soda or fruit juices (except orange and grapefruit juices because these are too acidic). Rest either in a sitting position or in a propped lying position. Activity may worsen nausea and may lead to vomiting. To prevent nausea and vomiting in children: To treat motion sickness in a car, seat your child so he or she faces the front windshield (watching fast movement out the side windows can make the nausea worse). Don't let your kids eat and play at the same time. Further Reading: Gastroenteritis Treatment Gastroenteritis Gastroenteritis, Eosinophilic Slideshow: Pictures of nausea & vomiting remedies The Truth About Stomach Flu Gastroenteritis in Adults and Older Children-Related Information

Gastroenteritis in Adults and Older Children-Topic Overview See All Gastroenteritis Topics Also Recommended: Is There a Product That Will Increase Fiber but Not Gas? Newly Diagnosed With Crohn's? Steps to Take Diarrhea: Three Types & Their Causes Abdominal Pain: What Could Be Causing It Foods That Can Be Problematic as You Age Is Acid Reflux Causing Your Cough? < Previous Page 1|2 WebMD Medical Reference View Article Sources SOURCES: National Institutes of Health. American Academy of Family Physicians. Reviewed by Venkat Mohan, MD on March 01, 2010 2010 WebMD, LLC. All rights reserved. Gastroenteritis Home Medical Reference Features Slideshows & Images News Archive Digestive Disorders Health Center Heartburn/GERD Inflammatory Bowel Disease

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What is liver failure?

Liver failure is a life-threatening condition in which there is a severe deterioration of liver function. The liver is a vital organ located in the right upper area of your abdomen under the ribs. Liver failure is caused by liver damage, which makes it difficult or impossible for the liver to function normally in processes that are critical to life and your overall health including:

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Blood clotting Clearing the blood of toxins Fighting infection Making bile that assists with digestion Metabolizing medications and other substances Producing proteins, enzymes, and healthy blood Removing waste Storing vitamins, minerals and energy Acute liver failure is a failure of liver function that occurs suddenly due to such conditions as an overdose of acetaminophen (Tylenol) or ingestion of toxic substances. Chronic liver failure is a deterioration of liver function that occurs over a long period of time, generally months to years. Chronic liver failure is the most common form of liver failure and is generally due to long-term liver diseases, such as cirrhosis of the liver and hemochromatosis.

There are two general types of liver failure:

Symptoms of early liver failure can be vague and similar to many other less serious diseases, such as chronic fatigue syndrome or viral gastroenteritis. A hallmark symptom of advancing liver failure is jaundice, a yellowing of the skin and whites of the eyes. In some cases of acute liver failure, rapid diagnosis and treatment may reverse the condition. However, once permanent liver damage has occurred due to either acute or chronic liver damage, it cannot be reversed or cured. Patient compliance with a good treatment plan may be able to slow or stop progression of liver damage and minimize complications. Liver failure is a life-threatening condition that is often fatal because it drastically affects the livers ability to function normally. Seek prompt medical care if you have a history of chronic disease, such as hepatitis, congestive heart failure, or cirrhosis of the liver, and unexplained symptoms, such as nausea, fatigue, diarrhea or weakness. In addition, if you have any form of liver disease or liver failure, do not take any supplements, over-the-counter medications or prescription drugs without consulting your health care provider. This is because the liver may not be able to clear the drugs from the body, resulting in dangerous, toxic levels of chemicals or and other harmful substances in the body. Seek immediate medical care (call 911) if you, or someone you are with, have symptoms of acute or advanced chronic liver failure, such as shakiness, jaundice, confusion, shortness of breath, abdominal swelling, or a change in consciousness or alertness. You should also seek immediate medical care (call 911) if you, or someone you are with, have overdosed on a drug or ingested a toxic substance.
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What are the symptoms of liver failure?

Early symptoms of liver failure are often not specific and may be confused with symptoms of many other conditions, such as indigestion, viral gastroenteritis, or chronic fatigue syndrome. Early symptoms may include:... Read more about liver failure symptoms
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What causes liver failure?

Liver failure is due to underlying liver diseases that often cause progressive damage to the liver. Liver disease generally begins with inflammation and enlargement of the liver, which may be reversed with medical treatment in some cases. Left untreated, liver inflammation leads to fibrosis (scarring) of the liver tissue that progresses and ultimately replaces healthy liver tissue. Scarred liver tissue cannot function normally, but prompt treatment may still reverse damage in some cases.... Read more about liver failure causes
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How is liver failure treated?

Scar tissue formed in the liver due to advanced liver disease, which causes liver failure, is permanent. The goal of treatment is to stop or slow the progression of damage to the liver and minimize and quickly treat any other complications and coexisting conditions, such as portal hypertension and hemorrhage. Treatment plans include a multifaceted and individualized approach that varies depending on the underlying cause of liver disease and liver failure. For example:... Read more about liver failure treatments
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Gastrointestinal Bleeding Green Stool Heartburn Heartburn/Gastroesophageal Reflux Disease (GERD) Hemochromatosis Hepatitis Hiatal Hernia Indigestion Infant Symptoms Inflammatory Bowel Disease Inguinal Hernia Intestinal Conditions Irritable Bowel Syndrome Lactose Intolerance Left Lower Quadrant Pain Liver Abscess Liver Disease Liver Failure Liver Inflammation Liver Pain Liver Symptoms Lower Abdominal Pain Mesenteric Adenitis Mucus Symptoms Mucus in Stool Nausea Obstructive Jaundice Pale Stool Pancreas Symptoms Pancreatitis Paralytic Ileus Pellagra Pencil Thin Stools Peptic Ulcer Poor Appetite Rectal Bleeding

Rectal Discharge Rectal Lump Spitting Blood Steatorrhea Stomach Ache Stomach Cramps Stomach Problems Stool Color Stool Odor Stool Symptoms Ulcerative colitis Upper Abdominal Pain Ventral Hernia Vomiting Vomiting Blood Wheat Intolerance White Stool Yellow Stool

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Abdominal Vascular Injuries

Author: Timothy H Pohlman, MD, FACS; Chief Editor: John Geibel, MD, DSc, MA more... Overview Workup Treatment

Updated: Feb 18, 2010 What would you like to print? Print this section Print the entire contents of

Background Problem Epidemiology Pathophysiology Presentation Indications Relevant Anatomy Contraindications Show All

Multimedia Library Tables References

Background
The incidence of abdominal vascular injuries in military conflicts is surprisingly low, generally less than 5% of all vascular injuries. In contrast, approximately 30% of all vascular injuries observed in civilians occur in the abdomen. This striking difference between combat vascular trauma and noncombat vascular trauma can be attributed to low-energy missiles from civilian handguns and short prehospital transit times in urban settings, thereby making it more likely that a civilian with penetrating abdominal vascular injury will survive long enough to reach surgical care.

Abdominal vascular injuries. Tangential gunshot injury to the inferior vena cava repaired by means of lateral venography (arrow).

Recent studies
In the treatment of ruptured abdominal aortic aneurysm, Kimball et al conducted a retrospective study comparing standard primary abdominal closure with the initial use of the open abdomen using the vacuum-pack technique followed by delayed abdominal closure.[1] The investigators identified 3 ischemia-reperfusion criteria that predicted mortality and which were also useful as surrogate clinical markers for abdominal compartment syndrome: preoperative hypotension, estimated blood loss of 6 L or greater, or intraoperative resuscitation with 12 L or more. Patients who had at least 1 of the 3 ischemia-reperfusion criteria had higher in-hospital mortality (43% vs 10%; P = .0003).[1] Of those who had at least 1 criterion, the initial 24-hour mortality as well as the 30-day mortality was higher in those with a primarily closed abdomen relative to those with a 47% open abdomen. In a in hypothermic traumatic shock swine model, Ding et al demonstrated that temporary intravascular shunts may improve survival in superior mesentery artery injuries compared with repair by primary vascular anastomosis.[2] Relative to pigs in the primary vascular anastomosis group, the animals treated with temporary shunting required less resuscitation fluid, retained higher superior mesenteric artery flow rates, normalized lactate levels faster, suffered less severe intestine histopathology, and had greater early survival.[2] Although the investigators caution that further research is needed, they believe that in the setting of superior mesenteric artery transection, temporary intravascular shunts show promise for better management of damage control surgery than primary vascular anastomosis.
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Problem
Injuries to major abdominal vessels are uncommon but highly lethal vascular crises. Predictably, exsanguinating hemorrhage is the most important cause of early death. Intra-abdominal vascular injuries are associated with extremely rapid rates of blood loss and pose challenges of exposure during celiotomy,[3, 4, 5] given the posterior position, except for the portal vein and the hepatic artery, of the major abdominal vascular structures. Essential to the successful management of these injuries is a thorough knowledge of the complex anatomy of intra-abdominal vascular structures and a familiarity with the techniques of proximal and distal control combined with selected application of primary repair, bypass, and/or ligation. Once exposure and proximal and distal control have been obtained, all abdominal vascular injuries should be graded using the American Association for the Surgery of Trauma-Organ Injury Scale for vascular injuries (AAST-OIS) (see the table below).

American Association for the Surgery of Trauma-Organ Injury Scale for Vascular Injuries (Open Table in a new window)
OIS

Artery Injured Grade*

Vein Injured

II

Hepatic

Splenic

Splenic

Inferior mesenteric

Gastric

Gastroduodenal

Inferior mesenteric

Primary named vessels of the SMA

III

Renal

Superior mesenteric

Iliac

Renal

Hypogastric

Iliac

Hypogastric

Vena cava (infrarenal)

IV

Superior mesenteric (trunk)

Vena cava (infrahepatic)

Celiac axis

Aorta (infrarenal)

Aorta (suprarenal)

Vena cava (suprahepatic)

Vena cava (retrohepatic)

Portal

Hepatic (extrahepatic)

Grade I injury includes the following: No named superior mesenteric artery or superior mesenteric vein branches. Non-named inferior mesenteric artery or inferior mesenteric vein branches. Phrenic artery/vein. Lumbar artery/vein. Gonadal artery/vein. Ovarian artery/vein. Other non-named small arterial or venous structures requiring ligation.
*

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Epidemiology
Frequency
The incidence of abdominal vessel injury in patients with blunt trauma is estimated at approximately 5-10%. A similar incidence of 10.3% is reported in patients with penetrating stab wounds to the abdomen. Patients with gunshot wounds (GSWs) to the abdomen will have major vessel injury in 20-25% of cases.
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Pathophysiology
In blunt trauma, rapid deceleration during a motor vehicle accident (MVA) results in an avulsion of the small branches of major vessels (eg, mesenteric tear). Another mechanism of injury is related to a direct crush or blow to the major vessels, resulting in an intimal tear with thrombosis or vessel rupture and hemorrhage. Penetrating injuries directly disrupt the vessel wall or create intimal flaps secondary to the blast effect. Because of the anatomical position of the major vascular structures in the abdomen, injuries to these vessels have a high probability of association with other major injuries in the abdomen, particularly to the small bowel. Hemorrhagic shock from intra-abdominal hemorrhage often leads to metabolic acidosis accompanied by coagulopathy and hypothermia, the so-called lethal triad of trauma. Metabolic acidosis in trauma patients is the result of lactate overproduction, most often from decreased oxygen delivery as a result of hypovolemic shock. Acidosis adds to the overall lethality of preexisting injury primarily by depression of myocardial contractility and by impairment of coagulation. Furthermore, hypothermia (below 34C) inhibits platelet function and slows coagulation factor activation. This self-perpetuating cycle is responsible for 80% of deaths in patients with major vascular injury and must be rapidly corrected to prevent a dismal outcome.
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Presentation
Clinical data obtained from emergency medical services (EMS) can be crucial and may be the only patient information available. In inner city hospitals, GSWs and stab wounds predominate. Mechanism of injury, vital signs at the scene of the accident, and transit time are essential. The amount of intravenous fluid the patient received in the field and during transport should also be elicited from EMS. Penetrating trauma to the chest below the nipple line should also be considered as penetrating trauma to the abdomen.
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Indications
Blunt trauma
Hemodynamically stable patients who have peritoneal signs or positive CT findings require exploration. Hemodynamically unstable patients with positive results, including pericardial effusion, on focused abdominal ultrasound for trauma (FAST) examination or diagnostic peritoneal lavage (DPL) require surgery.

Penetrating trauma
Evaluate stable patients with posterior wounds and most patients with anterior stab wounds with triple-contrast CT scanning (eg, oral, intravenous, rectal), diagnostic laparoscopy to exclude peritoneal penetration, and/or FAST examination to exclude hemoperitoneum. GSWs to the abdomen require celiotomy for evaluation and treatment, although some trauma surgeons prefer selective nonoperative evaluation of abdominal GSWs in stable patients. Hemodynamically unstable patients should be transported immediately to the operating room (OR) if the airway is secure and ventilation is adequate, preferably within 5 minutes of arrival to the emergency department (ED).
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Relevant Anatomy
The following anatomical locations should be distinguished:
Midline supramesocolic hemorrhage or hematoma (superior to the transverse mesocolon) is usually caused by injury to the suprarenal aorta, celiac axis, proximal superior mesenteric artery, or proximal renal artery. Midline inframesocolic hemorrhage or hematoma results from infrarenal aorta or inferior vena cava (IVC) injury. Lateral perirenal hematoma or hemorrhage suggests injury to the renal vessels or kidneys. Lateral pelvic hematoma or hemorrhage indicates injury to the iliac artery, iliac vein, or both. Hepatoduodenal ligament hematoma or hemorrhage indicates portal vein and/or hepatic artery injury.

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Contraindications
Patients without recorded vital signs at the scene of injury and blunt trauma victims without vital signs at the time of arrival to the ED rarely survive after resuscitation, with or without ED thoracotomy.
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Contributor Information and Disclosures Author

Timothy H Pohlman, MD, FACS Professor, Section of Trauma and Critical Care, Department of Surgery, Indiana University School of Medicine; Director, Surgical Critical Care, Methodist Hospital, Clarian Health Partners, Inc Timothy H Pohlman, MD, FACS is a member of the following medical societies: American College of Surgeons, Association for Academic Surgery, Society of University Surgeons, and Surgical Infection Society Disclosure: Nothing to disclose.
Coauthor(s)

H Scott Bjerke, MD, FACS Clinical Associate Professor, Department of Surgery, University of Missouri-Kansas City School of Medicine; Medical Director of Trauma Services, Research Medical Center; Clinical Associate Professor, Department of Surgery, Indiana University School of Medicine H Scott Bjerke, MD, FACS is a member of the following medical societies: American Association for the History of Medicine, American Association for the Surgery of Trauma, American College of Surgeons, Association for Academic Surgery, Eastern Association for the Surgery of Trauma, Midwest Surgical Association, National Association of EMS Physicians, Pan-Pacific Surgical Association, Royal Society of Medicine, Southwestern Surgical Congress, and Wilderness Medical Society Disclosure: Nothing to disclose. Aleksander R Komar, MD Fellow, Section of Trauma and Critical Care, SUNY Stony Brook Disclosure: Nothing to disclose. Richard Fogler, MD, DS, FACS Chair, Program Director, Department of Surgery, Division of Surgical Oncology, Brookdale University Hospital and Medical Center Richard Fogler, MD, DS, FACS is a member of the following medical societies: American College of Surgeons and American Society of Abdominal Surgeons Disclosure: Nothing to disclose.
Specialty Editor Board

Ernest Dunn, MD Program Director of General Surgery, Director of Trauma and Critical Care, Clinical Associate Professor, Department of Surgery, Methodist Hospitals of Dallas, University of Texas Southwestern

Ernest Dunn, MD is a member of the following medical societies: American College of Surgeons, American Medical Association, Association for Academic Surgery, Society of Critical Care Medicine, and Texas Medical Association Disclosure: Nothing to disclose. Francisco Talavera, PharmD, PhD Senior Pharmacy Editor, eMedicine Disclosure: eMedicine Salary Employment Robert L Sheridan, MD Assistant Chief of Staff, Chief of Burn Surgery, Shriners Burns Hospital; Associate Professor of Surgery, Department of Surgery, Division of Trauma and Burns, Massachusetts General Hospital and Harvard Medical School Robert L Sheridan, MD is a member of the following medical societies: American Academy of Pediatrics, American Association for the Surgery of Trauma, American Burn Association, and American College of Surgeons Disclosure: Nothing to disclose. Paolo Zamboni, MD Professor of Surgery, Chief of Day Surgery Unit, Chair of Vascular Diseases Center, University of Ferrara, Italy Paolo Zamboni, MD is a member of the following medical societies: American Venous Forum and New York Academy of Sciences Disclosure: Nothing to disclose.
Chief Editor

John Geibel, MD, DSc, MA Vice Chairman, Professor, Department of Surgery, Section of Gastrointestinal Medicine and Department of Cellular and Molecular Physiology, Yale University School of Medicine; Director of Surgical Research, Department of Surgery, YaleNew Haven Hospital John Geibel, MD, DSc, MA is a member of the following medical societies: American Gastroenterological Association, American Physiological Society, American Society of Nephrology, Association for Academic Surgery, International Society of Nephrology, New York Academy of Sciences, and Society for Surgery of the Alimentary Tract Disclosure: AMGEN Royalty Other
References

1. Kimball EJ, Adams DM, Kinikini DV, Mone MC, Alder SC. Delayed abdominal closure in the management of ruptured abdominal aortic aneurysm. Vascular. Nov-Dec 2009;17(6):309-15. [Medline]. 2. Ding W, Wu X, Pascual JL, et al. Temporary intravascular shunting improves survival in a hypothermic traumatic shock swine model with superior mesenteric artery injuries. Surgery. Jan 2010;147(1):79-88. [Medline].

3. Fabian TC. Abdominal trauma including indications for celiotomy. In: Feliciano DV, Moore EE, Mattox KL, eds. Trauma. 3rd ed. Norwalk, Conn: Appleton and Lange; 1996:441-59. 4. Cox EF. Blunt abdominal trauma. A 5-year analysis of 870 patients requiring celiotomy. Ann Surg. Apr 1984;199(4):467-74. [Medline]. 5. Morris JA, Eddy VA, Rutherford EJ. The trauma celiotomy: the evolving concepts of damage control. Curr Probl Surg. Aug 1996;33(8):611-700. [Medline]. 6. Feliciano DV. Abdominal vascular injury. In: Feliciano DV, Moore EE, Mattox KL, eds. Trauma. 3rd ed. Norwalk, Conn: Appleton and Lange; 1996:615-33. 7. Feliciano DV. Injuries to the great vessels of the abdomen. In: Wilmore DW, Cheung LY, Harken AH, Holcroft JW, Meakins JL, eds. Scientific American Surgery. New York, NY: Scientific American; 1996, revised 1998. 8. Vu M, Anderson SW, Shah N, Soto JA, Rhea JT. CT of blunt abdominal and pelvic vascular injury. Emerg Radiol. Jan 2010;17(1):21-9. [Medline]. 9. Boffard KD, Riou B, Warren B, et al. Recombinant factor VIIa as adjunctive therapy for bleeding control in severely injured trauma patients: two parallel randomized, placebocontrolled, double-blind clinical trials. J Trauma. Jul 2005;59(1):8-15; discussion 15-8. [Medline]. 10. DeBakey ME. Battle injuries of the arteries in WWII: an analysis of 2,471 cases. Ann Surg. 1946;123:534. 11. Feliciano DV, Burch JM, Spjut-Patrinely V, Mattox KL, Jordan GL Jr. Abdominal gunshot wounds. An urban trauma center's experience with 300 consecutive patients. Ann Surg. Sep 1988;208(3):362-70. [Medline]. 12. Jurkovich GJ, Hoyt DB, Moore FA, et al. Portal triad injuries. J Trauma. Sep 1995;39(3):426-34. [Medline]. 13. Pourmoghadam KK, Fogler RJ, Shaftan GW. Ligation: an alternative for control of exsanguination in major vascular injuries. J Trauma. Jul 1997;43(1):126-30. [Medline]. 14. Thal ER. Operative exposure of abdominal injuries and closure of the abdomen. In: Wilmore DW, Cheung LY, Harken AH, et al, eds. Scientific American Surgery. New York, NY: Scientific American; 1996, revised 1997.

Abdominal vascular injuries. Tangential gunshot injury to the inferior vena cava repaired by means of lateral venography (arrow). Table 1

Table 1 OIS

Artery Injured Grade*

Vein Injured

II

Hepatic

Splenic

Splenic

Inferior mesenteric

Gastric

Gastroduodenal

Inferior mesenteric

Primary named vessels of the SMA

III

Renal

Superior mesenteric

Iliac

Renal

Hypogastric

Iliac

Hypogastric

Vena cava (infrarenal)

IV

Superior mesenteric (trunk)

Vena cava (infrahepatic)

Celiac axis

Aorta (infrarenal)

Aorta (suprarenal)

Vena cava (suprahepatic)

Vena cava (retrohepatic)

Portal

Hepatic (extrahepatic)

Grade I injury includes the following: No named superior mesenteric artery or superior mesenteric vein branches. Non-named inferior mesenteric artery or inferior mesenteric vein branches. Phrenic artery/vein. Lumbar artery/vein. Gonadal
*

artery/vein. Ovarian artery/vein. Other non-named small arterial or venous structures requiring ligation.

View Table List

Read more about Abdominal Vascular Injuries on Medscape Related Reference Topics Abdominal Vascular Injuries Liver Trauma Imaging Considerations in Pediatric Trauma Related News and Articles Bullet Embolization to the External Iliac Artery After Gunshot Injury to the Abdominal Aorta Splenic Injury After Blunt Abdominal Trauma Prophylaxis and Treatment of Infections Associated with Penetrating Traumatic Injury

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Abdominal Vascular Injuries Treatment & Management

Author: Timothy H Pohlman, MD, FACS; Chief Editor: John Geibel, MD, DSc, MA more... Overview Workup Treatment

Updated: Feb 18, 2010 What would you like to print? Print this section Print the entire contents of

Medical Therapy Preoperative Details Intraoperative Details Postoperative Details Complications Outcome and Prognosis Show All

Multimedia Library Tables References

Medical Therapy
Initial resuscitation of a patient with abdominal vascular injuries depends on his or her condition at arrival to the ED. Insert multiple large-bore catheters into the upper extremities, or, if necessary, obtain central venous access for rapid infusion of warm isotonic fluid. Because a possibility of intra-abdominal venous injury exists, lower extremity venous access is not recommended. In the agonal patient with a distended abdomen suggesting major intraperitoneal bleeding, ED thoracotomy with cross clamping of the descending aorta may be necessary. This is usually associated with a poor prognosis and low survival rates. Perform blood replacement during resuscitation with type-specific blood if time permits receiving this blood in the ED. If time does not permit, use O-negative blood (or O-positive blood for males), which should be immediately available in the ED. Start efforts to limit

hypothermia as soon as the patient arrives. Ensure that prewarmed fluids, high-flow blood warmers, and prewarmed blankets are available.
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Preoperative Details
Place the patient on a warming blanket, and make every effort to reduce heat loss. Drape the patient to expose chest and both thighs in the event that a thoracotomy or vein harvest is required. Perform a generous midline incision from the xiphoid to well below the umbilicus, which can be extended to the pubis if needed to improve exposure. Aggressively administer blood replacement therapy. A radial arterial line may be helpful for monitoring blood pressure and arterial blood gases.

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Intraoperative Details
Enter the peritoneal cavity through a midline incision. Quickly evacuate blood and clots and perform 4-quadrant packing. After initial stabilization, systematically remove the packing and evaluate the injuries. Injuries to major abdominal vessels can be grouped into the following 5 regions:
Midline supramesocolic hemorrhage or hematoma (superior to the transverse mesocolon) This problem is usually from an injury to the suprarenal aorta, celiac axis, proximal superior mesenteric artery, or proximal renal artery. Use aortic compression to obtain proximal aortic control at the hiatus. Once aortic control is achieved, gain direct access to the vessels through retroperitoneal mobilization and medial rotation of all leftsided abdominal viscera (Mattox maneuver) or an extensive Kocher maneuver on the right side. An injured celiac axis may be safely ligated in critical situations. Access to the superior mesenteric artery and vein may require transection of the pancreas. Primary repair of this major vessel is usually the first choice; however, ligation, particularly of the venous structures, may be a better option. Significant venous congestion can compromise viability of the bowel. This problem results from infrarenal aortic or IVC injury. Obtain exposure by incising the posterior peritoneum in the midline after evisceration of the small bowel and cephalic retraction of the

Midline inframesocolic hemorrhage or hematoma

transverse mesocolon, or divide the white line of Toldt adjacent to the cecum and extend cephalad through the hepatic flexure followed by medial rotation of the right colon and small bowel (Cattel-Braasch maneuver). Place an aortic clamp just below the left renal vein and apply a distal clamp near the aortic bifurcation. The injury is primarily repaired. If the aorta is intact, suspect injury to the IVC and obtain access to the infrahepatic IVC by mobilizing the right colon and duodenum. Preferably, repair anterior injuries in transverse fashion. Posterior injuries can be repaired from inside the IVC. Both approaches require proximal and distal control of the vessel. Apply a Satinsky clamp or Judd Alyce clamp to the injury. Large IVC defects may be repaired by using a patch from the peritoneum. In patients with multiple injuries and exsanguinating hemorrhage, ligate the infrarenal IVC. This problem suggests injury to the renal vessels or kidneys. Exploration after blunt trauma is not necessary in patients with a negative result on abdominal CT scan, preoperative intravenous pyelogram, or arteriogram, or if the hematoma is not expanding. Penetrating injury usually indicates a necessity for exploration. Obtain vascular control of the ipsilateral renal artery. Expose the kidney and clamp the renal vessels if active bleeding from the kidney or an overlying retroperitoneum is present. Only 30-40% of kidneys with arterial injuries can be salvaged. Before performing a nephrectomy, assess the viability of the contralateral kidney. This problem indicates injury to the iliac artery, iliac vein, or both. Obtain vascular control at the aortic bifurcation proximally and close to the inguinal ligament distally. If an injury to the right common iliac vein is present, it may require a division of the overlying right common iliac artery. For best visualization of the internal iliac artery, elevate the common and external iliac arteries on vascular tapes. Repair injuries to the common or external iliac arteries. Treat injuries to the iliac veins with lateral venography or ligation. Once initial control of the hemorrhage is completed and gross contamination is controlled, terminate the procedure and transfer the

Lateral perirenal hematoma or hemorrhage

Lateral pelvic hematoma or hemorrhage

patient to the recovery room for further resuscitation. Measurement of abdominal compartment pressure may be needed. Hepatoduodenal ligament hematoma This problem indicates injury to the portal vein, hepatic artery, or both. Obtain vascular control by clamping the porta hepatis with vascular clamps proximal and distal to the injury (double Pringle maneuver). Portal vein ligation may be required to expeditiously manage portal vein injuries if the patient is exsanguinating, although primary repair may be attempted. Hepatic artery injuries are generally managed by ligation. If portal vein inflow is compromised, the liver should be assessed for ischemia, and restoration of hepatic arterial inflow or resectional debridement of the ischemic section should be undertaken or staged.

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Postoperative Details
Patients may require aggressive resuscitation involving the correction of acidosis, active rewarming, and massive blood transfusion (>10 U of blood within 24 h). Fresh frozen plasma, platelets, cryoprecipitate, or recombinant factor VIIa (rFVIIa) may be required on an individual basis to correct coagulopathy induced by massive transfusion. A planned reoperation 24-48 hours after the initial procedure is done to complete a damage control sequence.
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Complications
Early
Ongoing bleeding Coagulopathy Abdominal compartment syndrome Intra-abdominal infections Wound dehiscence Acute respiratory distress syndrome (ARDS) Pneumonia

Late

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Outcome and Prognosis

Mortality
Suprarenal aorta (60%) Superior mesenteric artery (40-80%) Superior mesenteric vein (20%) Combined injury to the suprarenal aorta and IVC (100%) Infrarenal abdominal aorta (50%) Infrarenal vena cava (30%) Renal artery (15%) Iliac artery (40%) Iliac vein (30%)

Previous Contributor Information and Disclosures Author

Timothy H Pohlman, MD, FACS Professor, Section of Trauma and Critical Care, Department of Surgery, Indiana University School of Medicine; Director, Surgical Critical Care, Methodist Hospital, Clarian Health Partners, Inc Timothy H Pohlman, MD, FACS is a member of the following medical societies: American College of Surgeons, Association for Academic Surgery, Society of University Surgeons, and Surgical Infection Society Disclosure: Nothing to disclose.
Coauthor(s)

H Scott Bjerke, MD, FACS Clinical Associate Professor, Department of Surgery, University of Missouri-Kansas City School of Medicine; Medical Director of Trauma Services, Research Medical Center; Clinical Associate Professor, Department of Surgery, Indiana University School of Medicine H Scott Bjerke, MD, FACS is a member of the following medical societies: American Association for the History of Medicine, American Association for the Surgery of Trauma, American College of Surgeons, Association for Academic Surgery, Eastern Association for the Surgery of Trauma, Midwest Surgical Association, National Association of EMS Physicians, Pan-Pacific Surgical Association, Royal Society of Medicine, Southwestern Surgical Congress, and Wilderness Medical Society Disclosure: Nothing to disclose.

Aleksander R Komar, MD Fellow, Section of Trauma and Critical Care, SUNY Stony Brook Disclosure: Nothing to disclose. Richard Fogler, MD, DS, FACS Chair, Program Director, Department of Surgery, Division of Surgical Oncology, Brookdale University Hospital and Medical Center Richard Fogler, MD, DS, FACS is a member of the following medical societies: American College of Surgeons and American Society of Abdominal Surgeons Disclosure: Nothing to disclose.
Specialty Editor Board

Ernest Dunn, MD Program Director of General Surgery, Director of Trauma and Critical Care, Clinical Associate Professor, Department of Surgery, Methodist Hospitals of Dallas, University of Texas Southwestern Ernest Dunn, MD is a member of the following medical societies: American College of Surgeons, American Medical Association, Association for Academic Surgery, Society of Critical Care Medicine, and Texas Medical Association Disclosure: Nothing to disclose. Francisco Talavera, PharmD, PhD Senior Pharmacy Editor, eMedicine Disclosure: eMedicine Salary Employment Robert L Sheridan, MD Assistant Chief of Staff, Chief of Burn Surgery, Shriners Burns Hospital; Associate Professor of Surgery, Department of Surgery, Division of Trauma and Burns, Massachusetts General Hospital and Harvard Medical School Robert L Sheridan, MD is a member of the following medical societies: American Academy of Pediatrics, American Association for the Surgery of Trauma, American Burn Association, and American College of Surgeons Disclosure: Nothing to disclose. Paolo Zamboni, MD Professor of Surgery, Chief of Day Surgery Unit, Chair of Vascular Diseases Center, University of Ferrara, Italy Paolo Zamboni, MD is a member of the following medical societies: American Venous Forum and New York Academy of Sciences Disclosure: Nothing to disclose.
Chief Editor

John Geibel, MD, DSc, MA Vice Chairman, Professor, Department of Surgery, Section of Gastrointestinal Medicine and Department of Cellular and Molecular Physiology, Yale University School of Medicine; Director of Surgical Research, Department of Surgery, YaleNew Haven Hospital

John Geibel, MD, DSc, MA is a member of the following medical societies: American Gastroenterological Association, American Physiological Society, American Society of Nephrology, Association for Academic Surgery, International Society of Nephrology, New York Academy of Sciences, and Society for Surgery of the Alimentary Tract Disclosure: AMGEN Royalty Other
References

1. Kimball EJ, Adams DM, Kinikini DV, Mone MC, Alder SC. Delayed abdominal closure in the management of ruptured abdominal aortic aneurysm. Vascular. Nov-Dec 2009;17(6):309-15. [Medline]. 2. Ding W, Wu X, Pascual JL, et al. Temporary intravascular shunting improves survival in a hypothermic traumatic shock swine model with superior mesenteric artery injuries. Surgery. Jan 2010;147(1):79-88. [Medline]. 3. Fabian TC. Abdominal trauma including indications for celiotomy. In: Feliciano DV, Moore EE, Mattox KL, eds. Trauma. 3rd ed. Norwalk, Conn: Appleton and Lange; 1996:441-59. 4. Cox EF. Blunt abdominal trauma. A 5-year analysis of 870 patients requiring celiotomy. Ann Surg. Apr 1984;199(4):467-74. [Medline]. 5. Morris JA, Eddy VA, Rutherford EJ. The trauma celiotomy: the evolving concepts of damage control. Curr Probl Surg. Aug 1996;33(8):611-700. [Medline]. 6. Feliciano DV. Abdominal vascular injury. In: Feliciano DV, Moore EE, Mattox KL, eds. Trauma. 3rd ed. Norwalk, Conn: Appleton and Lange; 1996:615-33. 7. Feliciano DV. Injuries to the great vessels of the abdomen. In: Wilmore DW, Cheung LY, Harken AH, Holcroft JW, Meakins JL, eds. Scientific American Surgery. New York, NY: Scientific American; 1996, revised 1998. 8. Vu M, Anderson SW, Shah N, Soto JA, Rhea JT. CT of blunt abdominal and pelvic vascular injury. Emerg Radiol. Jan 2010;17(1):21-9. [Medline]. 9. Boffard KD, Riou B, Warren B, et al. Recombinant factor VIIa as adjunctive therapy for bleeding control in severely injured trauma patients: two parallel randomized, placebocontrolled, double-blind clinical trials. J Trauma. Jul 2005;59(1):8-15; discussion 15-8. [Medline]. 10. DeBakey ME. Battle injuries of the arteries in WWII: an analysis of 2,471 cases. Ann Surg. 1946;123:534. 11. Feliciano DV, Burch JM, Spjut-Patrinely V, Mattox KL, Jordan GL Jr. Abdominal gunshot wounds. An urban trauma center's experience with 300 consecutive patients. Ann Surg. Sep 1988;208(3):362-70. [Medline]. 12. Jurkovich GJ, Hoyt DB, Moore FA, et al. Portal triad injuries. J Trauma. Sep 1995;39(3):426-34. [Medline].

13. Pourmoghadam KK, Fogler RJ, Shaftan GW. Ligation: an alternative for control of exsanguination in major vascular injuries. J Trauma. Jul 1997;43(1):126-30. [Medline]. 14. Thal ER. Operative exposure of abdominal injuries and closure of the abdomen. In: Wilmore DW, Cheung LY, Harken AH, et al, eds. Scientific American Surgery. New York, NY: Scientific American; 1996, revised 1997.

Abdominal vascular injuries. Tangential gunshot injury to the inferior vena cava repaired by means of lateral venography (arrow). Table 1

Table 1 OIS

Artery Injured Grade

*

Vein Injured

II

Hepatic

Splenic

Splenic

Inferior mesenteric

Gastric

Gastroduodenal

Inferior mesenteric

Primary named vessels of the SMA

III

Renal

Superior mesenteric

Iliac

Renal

Hypogastric

Iliac

Hypogastric

Vena cava (infrarenal)

IV

Superior mesenteric (trunk)

Vena cava (infrahepatic)

Celiac axis

Aorta (infrarenal)

Aorta (suprarenal)

Vena cava (suprahepatic)

Vena cava (retrohepatic)

Portal

Hepatic (extrahepatic)

Grade I injury includes the following: No named superior mesenteric artery or superior mesenteric vein branches. Non-named inferior mesenteric artery or inferior mesenteric vein branches. Phrenic artery/vein. Lumbar artery/vein. Gonadal artery/vein. Ovarian artery/vein. Other non-named small arterial or venous structures requiring ligation.
*

View Table List

Read more about Abdominal Vascular Injuries on Medscape Related Reference Topics Abdominal Vascular Injuries Liver Trauma Imaging Considerations in Pediatric Trauma Related News and Articles Bullet Embolization to the External Iliac Artery After Gunshot Injury to the Abdominal Aorta Splenic Injury After Blunt Abdominal Trauma Prophylaxis and Treatment of Infections Associated with Penetrating Traumatic Injury

Medscape Reference 2011 WebMD, LLC

The Radiology Assistant

Home Abdomen Breast Cardiovascular Chest Head Neck Musculoskeletal Pediatrics Neuroradiology Miscellaneous Cases Top Sites Newsletter

Rectum - Perianal Fistulas

by Susanne Tonino and Robin Smithuis
Radiology Department of the Medical Centre Alkmaar and the Rijnland hospital, Leiderdorp, the Netherlands.

Anatomy Perianal fistula Classification MR Protocol and Reporting Examples of Perirectal Fistulas Intersphincteric fistula Transsphincteric fistula Extrasphincteric fistula Complex fistula Crohn's disease Treatment Differential diagnosis

back to overview Publicationdate 21-1: 2009

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Perianal fistula is a common disorder that often recurs because infection that was missed at surgery. Preoperative MR can help to prevent recurrence. In this review we will address the anatomy, pathogenesis, classification and scanning protocol of perianal fistulas. <BR< div < view. enlarged an get to images the on click can You>

Anatomy

The anatomical anal canal extends from the perineal skin to the linea dentata. Surgically, the anal canal extends from the perineal skin to the anorectal ring. This is the circular upper border of the puborectal muscle which is digitally palpable upon rectal examination. The anorectal ring lies approximately 1-1,5 cm above the linea dentata. The total length of the surgical anal canal is about 4-5 cm. The anal sphincter is comprised of three layers:

Internal sphincter: continuance of the circular smooth muscle of the rectum, involuntary and contracted durin rest, relaxes at defecation. Intersphincteric space. External sphincter: voluntary striated muscle, divided in three layers that function as one unit. These three layers are continuous cranially with the puborectal muscle and levator ani (figure).

The puborectal muscle has its origin on both sides of the pubic symphysis, forming a 'sling' around the anorectum.

Puborectal muscle forming a 'sling'

The puborectal muscle is contracted at rest and accounts for the 80 angulation of the anorectal junction. It relaxes during defecation.

On axial and coronal MR-images the different layers of the anal sphincter and the surrounding structures can be displayed perfectly.

Coronal T2W-image

Perianal fistula
A perianal fistula is an abnormal connection between the epithilialised surface of the anal canal and the skin. The causes of perianal fistulas: Primary

Obstruction of anal gland which leads to stasis and infection with absces and fistula formation (most common cause). Secondary Iatrogenic (hemorrhoideal surgery) Inflammatory bowel diseases (Crohn's disease more common than colitis ulcerosa) Infections (viral, fungal or TB) Malignancy

Classification The most widely used classification is the Parks Classification which distinguishes four kinds of fistula: intersphincteric, transsphincteric, suprasphincteric and extrasphincteric. The most common fistulas are the intersphincteric and the transsphincteric. The extrasphincteric fistula is uncommon and only seen in patients who had multiple operations. In these cases the connection with the original fistula tract to the bowel is lost.

A superficial fistula is a fistula that has no relation to the sphincter or the perianal glands and is not part of the Parks classification. These are more often due to Crohns disease or anorectal procedures such as haemorrhoidectomy or sphincterotomy.

MR Protocol and Reporting

Protocol A localizer in three directions is needed in order to align the T2 sequences axial and coronal to the anal canal. Any localizer that properly displays the anal canal can be used. We use a TRUE FISP, which is the name that Siemens uses for a steady-state precession gradient-echo sequence (GE: FIESTA, Philips: balanced FFE).

T2W images without fatsat better display the anatomy, while the fatsat images better depict the fistulas.

Perianal fistula: axial T2WI without fatsat (left) and with fatsat

(right) Reporting When you describe a fistula, it is important to mention the following characteristics:

Position of the mucosal opening on axial images (using the anal clock). Distance of the mucosal defect to the perianal skin on coronal images. Secondary fistulas or abscesses.

The drawing on the left illustrates the anal clock, which is the surgeon's view of the perianal region when the patient is in the supine lithotomy position (2). This scheme corresponds to the orientation of axial MR images of the perianal region.

Examples of Perirectal Fistulas

Intersphincteric fistula On the left axial T2W images with and without fat saturation. An intersphincteric fistula is located at 6 o'clock. Continue with coronal images.

On the coronal image the fistula runs caudally towards the skin. There is no connection with the external sphincter.

On the left coronal images of another patient with an intersphincteric fistula. Use the arrows to scroll through the images.

View more images:

1/6

Use the arrows to scroll through the images.

Transsphincteric fistula On the left an axial T2WI and T2WI + fatsat of a transsphincteric fistula. The defect through the internal and external sphincter at 6 o'clock is clearly visible and more apparent on the fat sat images.

Transsphincteric fistula with sphincter defect at 6 o'clock On the left axial T2W-fatsat images of a transsphincteric fistula with the mucosal opening at 11 o'clock.

Transsphincteric fistula with sphincter defect at 11 o'clock

On the left an example of a suprasphincteric fistula. There are two tracts in the ischioanal region. The right sided tract runs over the puborectal muscle (asterisk) and the mucosal opening lies at the level of the linea dentata (black arrow).

Extrasphincteric fistula On the left coronal T2W-images of a small abscess in the left ischioanal fossa, the fistula runs through the levator ani. It is therefore above the sphincter complex and extrasphincteric.

Complex fistula On the left an example of a complex fistula. Two tracts in the left buttock form a single tract (no. 1-2). This fistula breaks through the external sphincter (no. 4). In the intersphincteric space it divides again into two tracts (no. 5). One ends blindly in the intersphincteric space (no. 6). The other breaks through the internal sphincter with the mucosal defect at 1 o'clock.

View more images:

1/6

Use the arrows to scroll through the images.

Crohn's disease On the left a patient with a perianal fistula who has Crohn's disease. Continue with the coronal images.

On the coronal images the thickening of the bowel wall is demonstrated.

Axial fatsat images depict the transmural inflammation with infiltration of the mesenteric fat.

Treatment

Treatment is focussed on the elimination of the primary and secondary tracts, prevention of recurrence and to retain continence. The treatment given depends on the anatomy of the fistula, if it is a simple fistula with a low mucosal defect is can be probed in the OR to identify the mucosal defect at the linea dentata, then the tract can be opened. This is only possible if the external sphincter is not involved. Seton fistulotomy is a technique where a rubber ligature or vessel loop is pulled through the fistula, it then is tightened every 2 weeks or so in order to obtain pressure necrosis so that the Seton is slowly pulled through the muscle. This has the advantage that the muscle is slowly cut and fibroses at the same time in order to cause as little damage as possible to the sphincter complex. If there is an extrasphincteric fistula, the lower part is opened. The mucosal defect, which is by definition in the rectum, is then surgically closed. This patient was already known to have an intersfincteric fistula, the mucosal defect is at 1 o'clock. In the tract there is a linear structure with a low signal intensity. This is the Seton which was inserted to treat the fistula.

Differential diagnosis
Sinus pilonidalis On the left an example of a sinus pilonidalis. There is a small abscess just above the nates. There is no relation with the sphincter complex.

Sinus pilonidalis

Proctitis On the left images of a patient who presented with anal complaints. No fistula was seen. There is, however, a diffuse thickening of the rectal mucosa due to a proctitis.

Abscess in the Ischioanal space An abscess in the ischioanal space with no connection to the sphincter complex

Perianal abscess References

1. Imaging of Fistula in Ano

Halligan, Stoker et al. Radiology 2006;239:18-33 2. MR Imaging Classification of Perianal Fistulas and Its Implications for Patient Management. by John Morris Radiographics. 2000;20:623-635 3. MRI of Perianal Crohn's Disease by Karin Horsthuis and Jaap Stoker