T. Andrew Bowdle, MD, PhD

• Professor of Anesthesiology and Pharmaceutics
• Chief of the Division of Cardiothoracic Anesthesiology
• Department of Anesthesiology
• University of Washington
• Seattle, Washington

In its most fulminant form anxiety symptoms in kindergarten order buspirone without prescription, apoplexy may cause blindness anxiety and high blood pressure buy buspirone 10 mg amex, haemodynamic instability anxiety 4am proven buspirone 10 mg, coma anxiety 3000 generic 10 mg buspirone overnight delivery, and death venom separation anxiety cheap 5 mg buspirone overnight delivery. Patients without confusion or visual disturbance generally do well without surgery. Assess pituitary function once the acute illness has resolved, and treat as necessary. A scoring system has been suggested by the Society for endocrinology for the assessment of severity of apoplexy, which could serve as a tool for monitoring of conservatively managed patients (see Table 9. This system could also be used as an aid to auditing outcomes in surgically and conservatively managed patients. Clinical Endocrinology, 2011; 74(1): 920, with permission from John Wiley and Sons. Complete loss of hormone secretion can rapidly become life-threatening and requires immediate therapy. Presentation In the absence of stress, patients with severe hypopituitarism may have few symptoms or signs. Features include failure of lactation (deficiency of prolactin and oxytocin), failure of menstruation (lack of gonadotrophins), non-specific features. Examination · examination of the comatose patient is discussed under E Coma: assessment, pp. Investigations · General investigations for patients in coma are discussed under E Coma: assessment, pp. Management · General measures are as for any patient in coma (E Coma: assessment, pp. Bilateral tumours are more likely to represent part of a familial syndrome, and tumour location, as well as risk of malignancy, varies depending on the genetic defect. Presentation · Classically a triad of episodic headaches, sweating, and tachycardia. These are more sensitive and specific than catecholamines, and falsenegative results are rare. Measurements of 24h urine catecholamines remain useful and should be collected if metanephrine measurement is unavailable. If plasma metanephrines are unavailable, plasma catecholamines should be collected from an indwelling cannula placed over 30min previously in a supine patient. Tumour -stimulation may produce excessive vasodilatation and hypotension, requiring inotropic support. Protocol using oral phenoxybenzamine to prepare patients with catecholamine-secreting phaeochromocytoma and paraganglioma for surgery. History · · · · · · · · · · · · · Duration and severity (nocturia, frequency, water consumption at night). Measure urinary Na+ and K+ (random spot samples will give an indication of the loss of Na+ or K+ initially, and if losses are great, accurate timed samples of <6h are possible). If anterior pituitary hormones are abnormal, do not perform a water deprivation test, as both cortisol and thyroid deficiency impair excretion of free water. Weigh the patient at times 0, 4, 5, 6, 7, and 8h into the test (stop the test if >3% of body weight is lost). Interpretation · Normal response: urine osmolality rises to >750mOsm/kg with a small rise after desmopressin. The incidence is 1:15 000, with a mortality which has significantly reduced from 80% down to <10% due to better treatment and i awareness of the condition. The cause is unknown but may involve abnormal Ca2+ homeostasis in skeletal muscle cells. The condition seems to be inherited in an autosomal dominant manner, with variable penetrance. Diagnosis · Malignant hyperthermia most commonly presents in patients in their early 20s. Infusions should be repeated until cardiovascular and respiratory symptoms stabilize. Dopaminergic and -adrenergic agonists reduce heat dissipation and should be avoided. This syndrome is clinically distinct from malignant hyperthermia (E Malignant hyperthermia, pp. Clinical features Muscular rigidity, including dysphagia, dysarthria-early (96%). The syndrome can occur within hours of initiating drug therapy but typically takes 71 week. Differential diagnosis · · · · · · · Malignant hyperthermia (E Malignant hyperthermia, pp. Bromocriptine, amantadine, levodopa (increase dopaminergic tone and reduce rigidity, thermogenesis, and extrapyramidal symptoms). Most agents are used on the basis of experience or anecdotal evidence, with little supporting evidence. This group of patients has the highest rate of serious complications and mortality as a result of their severe disease. Painful (vaso-occlusive) crisis · this is the most common presentation in adults and children. Priapism · · · · prolonged, painful erections due to local vaso-occlusion (1­24h long). Some patients prefer pethidine, but there is a risk of seizures as the drug metabolites accumulate. Give oxygen · not of proven benefit (except in chest crises), but often provides symptomatic relief. Review sources of sepsis · Infections are frequent (at least partly due to hyposplenism). Give other supportive therapy Laxatives, antiemetics, and anti-pruritics with opiates. Extended red cell phenotyped transfusion Viral pCr Cross-match Exchange transfusion the exchange can be performed on a cell separator. If a larger exchange is not required or fluid balance is not precarious, manual venesection of 1­2U can be performed. Fluid replacement (normal saline 1L over 2­4h), followed by transfusion of extended phenotype cross-matched blood. An abnormality of any of these components may present as easy bruising, purpura, or spontaneous or excessive bleeding. Management General measures · Avoid non-steroidal medications, especially aspirin. D-dimers) and are therefore suggestive of widespread clot formation and breakdown. Transfuse only if there is continued bleeding or in preparation for major surgery. Immune-mediated thrombocytopenia · platelet transfusions are usually ineffective as sole therapy and rarely indicated, unless severe bleeding or urgent surgery required. Start the infusion very slowly, as anaphylactic reactions (fever, urticaria, bronchospasm, and hypotension) are not uncommon. Surgery · Depends on the surgery, but generally aim for platelet count >50 × 109/L. Reduced platelet production (chronic, stable) · If no bleeding, transfuse if count <10 × 109/L. Platelet transfusion · A single unit is either a pool of four buffy coats or platelets from a single donor from apheresis. Non-vitamin K antagonist oral anticoagulants renal impairment and drug interaction may exacerbate bleeding. However, their plasma half-life is longer and they are less effectively reversed with protamine. Severe haemorrhage should be managed with: · Supportive measures (blood transfusion). The abnormalities most commonly found are: · Obstructive jaundice: prolonged pT (vitamin K deficiency). Massive transfusion/cardiopulmonary bypass · Dilutional thrombocytopenia and coagulopathy usually occur once red cell concentrates equivalent to 72 blood volumes have been transfused. With cardiopulmonary bypass, the extracorporeal circuit further damages the native platelets and depletes coagulation factors. Clinical presentation depends upon the degree of factor deficiency and whether inherited or acquired. If inherited: · patients with <1% activity (= severe disease) have a serious bleeding diathesis. Acute presentations · Acute haemarthroses: often occur at sites of previous bleeding, particularly if this has led to degenerative joint disease. Symptoms include local tenderness, warmth, and swelling, and may take days or weeks to resolve. Iliopsoas bleed causes entrapment of the femoral nerve and produces the triad of groin pain, hip flexion, and sensory loss over the femoral nerve distribution. Investigations Generally, acute investigations are not necessary for simple joint and muscle bleeds in a known haemophiliac. The exact pathogenesis varies, but in each case microthrombi cause organ damage, and thrombocytopenia and depleted clotting factors result in bleeding. Massive transfusion may exacerbate coagulopathy by dilution of coagulation factors and platelets. There is little evidence that measures to prevent thrombosis (heparin, antithrombin) or to prevent thrombolysis improve the general prognosis. The clinical picture tends to vary with age, with renal abnormalities being more common in children and neurological problems in adults, but with considerable overlap. With aggressive and early plasma exchange, mortality is now <15%, but relapses are frequent and reduced with rituximab. Presentation Red cell problems · Anaemia: caused by replacement of normal erythropoiesis by leukaemia cells; also by bleeding due to low platelets or deranged clotting (ApL). Give O2: where possible, use a pulse oximeter to monitor O2 saturation, avoiding arterial puncture with thrombocytopenia. Treat immediate problems · Infection: until the blood film has been reviewed by a haematologist, assume the patient is neutropenic and treat all infections aggressively (E the febrile neutropenic patient 1, p. Confirmation of diagnosis · Take a full history, looking for possible aetiological factors. Most patients with ApL survive long term if they do not succumb to acute bleeding. The impact of the diagnosis on often young patients and their families is devastating, and extensive time is needed in discussion; this should be done by a haematologist. When desired by the patient, every attempt must be made to provide for banking of sperm collection prior to starting chemotherapy. Unfortunately, in practice, the presence of leukaemia itself often makes sperm non-viable, and the need to start treatment precludes repeated collections. Discussion about side effects patients need to be warned about hair loss, sterility, emesis (less of a problem with current antiemetics but varies with individual), infections, bleeding, mucositis, secondary cancers, etc. The patients are very reliant on close medical and nursing surveillance to ensure that they do not perish from preventable/treatable causes. Even if the neutrophil count is normal, treat the patients as being neutropenic, as they will have poorly functioning lymphocytes and low antibody production. Antiemetics usually required: lorazepam 1­2mg q8­12h; metoclopramide 10­20mg q6­8h; or ondansetron 4­8mg q12h. Venoocclusive disease presents as hepatomegaly, jaundice, and weight gain in the early post-transplant period. Management Supportive treatment: O2, diuretics (if pulmonary oedema), and ventilatory support. Cover for infectious causes with broad-spectrum antibiotics, antifungal agents, or occasionally antiviral agents (if viral respiratory tract infection is suspected). Deteriorating renal function Causes · Drug therapy (ciclosporin, amphotericin, aminoglycosides, chemotherapy, aciclovir, allopurinol). Management Supportive therapy with blood and platelet transfusion and hydration is usually sufficient. Discuss with urologists if severe, as more specialist intervention, such as bladder irrigation, may be required. Severely ill patients and those on steroids may not be able to mount a fever; signs such as tachypnoea, tachycardia, or hypotension should be considered serious. Basic microbiological investigations · Blood cultures: taken from Hickman line and by venepuncture. Important points · Antibiotic therapy should never be delayed to await further assessment of clinical progress or laboratory results. Central lines and urinary catheters should be inserted with platelet cover, and arterial puncture is best avoided (use pulse oximetry). Antimicrobial regimen When in doubt, take haematological advice; use the hospital policy. Monotherapy is usually inappropriate, even when an organism has been isolated; the patient may well have >1 infection. Duration of neutropenia is an important factor, as fungal infections become more likely the longer the period of neutropenia. It is effectively prevented and treated with aciclovir; the main complication is bacterial super-infection. Have a high index of suspicion and treat aggressively with amphotericin or fluconazole. There is extensive local tissue destruction with cavitating lung lesions or bone destruction of sinuses.

A linear dural opening of only a few millimeters is sufficient to identify the filum terminale anxiety eye symptoms buy buspirone 5 mg online, which is slightly grayer than cauda equina nerve roots and has very characteristic tortuous pial arteries anxiety symptoms 8dp5dt buy buspirone with a mastercard. Care must be taken to separate the filum from any adherent rootlets and to cauterize its pial vasculature before transecting it anxiety symptoms breathing problems cheap 5 mg buspirone fast delivery, because the cut end will often retract out of view anxiety symptoms brain zaps generic buspirone 10 mg on line. The intra-thecal space should be gently flushed with irrigation fluid prior to linear primary closure using a resilient permanent suture anxiety symptoms red blotches buspirone 10 mg buy on-line. A thin continuous layer of dural sealant is often used to supplement the dural closure. Depending on the age of the patient, the laminoplasty bone may be replaced with suture or with a small laminar plating system. Tethered cord syndrome refers to a variable constellation of symptoms that may include neurological, musculoskeletal, gait, voiding, and pain components. Distal thoracolumbar syringes provide additional indirect imaging evidence of a tethered spinal cord (but in isolation may be clinically insignificant). Patients undergoing spinal cord detethering generally have clearly documented tethered cord syndrome as well as imaging evidence of an anatomically tethered spinal cord. In cases of diagnostic uncertainty, particularly with isolated medically refractory voiding dysfunction, urodynamic testing by an experienced pediatric urologist can identify a neurogenic pattern of bladder dysfunction suggestive 36 Spinal Cord Tethering of tethered cord: detrusor-sphincter dyssynergia, reduced bladder compliance and volume, bladder hyperreflexia, and/or reduced sensation. Opening the lumbar theca in the presence of a significant Chiari I malformation can cause symptomatic worsening of the Chiari and, rarely, clinical decompensation. Many pediatric neurosurgeons choose to decompress a Chiari I malformation when present prior to spinal cord detethering. This can be done either under the same anesthetic or as a separate surgical encounter. However, if a conus medullaris-proximal filum cyst accompanies filum tethering, filum transection can be carried out at the caudal end of the cyst, accompanied by cyst fenestration. The patient should be definitively confirmed to have returned to their pre-operative functional and gait status. Routine peri-operative antibiotics are generally given, but not continued more than 24 hours post-operatively. Unless a pre-operative syrinx was present, no additional imaging is needed in the follow-up of a clinically well patient. Complications and Management Urinary retention and constipation are common, generally transient, complications of surgery for filum terminal transection. Urinary retention likely results from a combination of recumbency, pain and narcotic medication. However, excessive traction on the filum during surgery or injury to sacral nerve roots may very rarely contribute to temporary even permanent dysfunction. Lumbar pseudomeningocele with headache, or more rarely with minor neurological compromise from entrapped nerve roots, or frank spinal fluid leak, occur in a very tiny fraction of patients. Patients should be carefully warned about leak, and treated emergentlyifitoccurs,topreventinfection. Late spinal instability at the level of surgery, if the facet joints are left intact, is relatively unheard of after this operation. Careful peri-operative assessment and long-term follow-up of voiding dysfunction will protect both bladder and renal function. If filum tethering is associated with the presence of a distal spinal syrinx, follow up imaging should be obtained a few months after surgery to make sure that the syrinx size is stable to reduced. Syrinx re-imaging should also be obtained in the (rare) event of a symptomatic recurrence after filum detethering, looking for late syrinx expansion. Most controversial is the question of whether frank imaging abnormalities of the filum terminale and/or a frankly low position of the conus medullaris are always required to recommend surgery. In routine clinical practice, an asymptomatic thickened filum terminale is often diagnosed in infants or young children based on the occurrence of external lumbosacral stigmata of dysraphism (most commonly a sacral dimple). The diagnosis of filum abnormalities, with or without a low conus medullaris, may be important in avoiding the gradual onset of sensorimotor complaints of the distal lower extremities, delay in gross motor developmental milestones, such as cruising or walking, and avoidance of secondary incontinence and voiding dysfunction. However, the benefits of surgery in this circumstance are unproven, and delay of surgery until the occurrence of symptoms in later childhood is rarely associated with permanent or serious neurological or urological dysfunction. Furthermore, there is no high-quality prospective evidence regarding the appropriate timing of surgical intervention for minor occult dysraphism such as a thickened filum terminale, nor a full understanding of what proportion of such children might avoid surgery altogether without consequence. Predictors of urinary continence following tethered cord release in children with occult spinal dysraphism. Clinical significance of imaging and histological characteristics of filum terminale in tethered cord syndrome. Radiographic and clinical outcome of syringomyelia in patients treated for tethered cord syndrome without other significant imaging abnormalities. Comparison of section of filum terminale and non-neurosurgical management for urinary incontinence in patients with normal conus position and possible occult tethered cord syndrome. He had no history of urinary tract infections; however, his mother described difficulty with bowel movements since birth. Examination of the anal and perianal region demonstrated a paraspinal hemangioma and a small skin tag in the midline. A sacral fat pad is noted superior to the hemangioma and the gluteal cleft was asymmetric and deviated to the right side. The differential diagnosis also includes other forms of occult spinal dysraphism, tethered cord associated with possible fatty filum, spinal lipoma, or diastematomyelia. Physical examination is key for early diagnosis of occult spinal dysraphism: always inspect for atypical sacral dimples, hairy patches, hemangiomas, asymmetric gluteal clefts, fat pads in the lumbosacral region, and other abnormal masses. Infants < 5 months of age can undergo a non-invasive lumbar ultrasound preliminarily. Many infants diagnosed will present with a normal neurologic examination; however, progressive neurologic deficit or bowel/bladder dysfunction is common and thus surgery prior to deterioration is important. Cutaneous markers are often hints to underlying dysraphism and neonates are commonly neurologically asymptomatic. T1 weighted imaging will demonstrate any associated fatty components, as well as fat associated with the filum or conus. T2 weighted imaging is important for delineation of the conus, nerve roots, and filum. High-quality axial T1 and T2 imaging may be helpful for evaluating any fatty tract traveling through dysraphic elements and the anatomical relationship to the conus. It is important to image the entire spine as dysraphism can be present at multiple levels, although this is uncommon. Spinal dysraphism is also associated with other findings, such as syringomyelia or Chiari malformation. Urinary continence is more likely to be preserved in children if operated on prior to 1 year of age (80% versus 50%). If the patient presents with progressive deficits, surgery should be scheduled expeditiously but is rarely urgent or emergent. The surgeon and anesthesiologist must communicate that neurophysiologic monitoring is being performed and ensure that no paralytics are given and the appropriate anesthetic is utilized. The skin incision should be long enough to incorporate the craniocaudal dimensions of the lipomatous malformation. The high-powered microscope is used during all microdissection of the lipoma from the placode and intradural detethering. Identification of the lipoma-placode interface is easier in symmetric lesions than in asymmetric lesions. Once safe removal and detethering are accomplished, attention is then turned to dural closure. Some surgeons favor dural sealant as an additional bolster to a watertight closure. Laminoplasty is performed with small plates and screws in the older child whereas in the younger patient, the surgeon may prefer to use permanent suture. After copious irrigation with antibiotic impregnated solution, the lumbodorsal fascia is closed in a watertightfashion. Bladder and bowel dysfunction remain the primary morbidity in this patient population and intervention at or before first symptom onset is recommended. Any superficial infection should be appropriately managed prior to surgical intervention if there is no intradural infection. The indwelling Foley catheter is often kept in place while the patient remains flat in bed. After the Foley catheter is removed, it is important to ensure the patient can urinate and check post-void residuals. After the patient is allowed to ambulate, one should inspect for any sign of pseudomeningocele. Complications and Management Urinary dysfunction and constipation are common, generally transient, complications of this intervention. Retention is probably multi-factorial, resulting from the surgical procedure, the use of opioid pain medication, recumbency, and trauma from the Foley catheter. Urological consultation and replacement of the Foley catheter may be necessary in rare cases of severe retention. An aggressive bowel regimen can help with post-operative constipation, which is also likely to be multifactorial in nature. Wound infection and flap necrosis may be a higher risk in these patients because of large defects created with subcutaneous lipoma resection. To prevent this, many neurosurgeons will opt to avoid aggressive removal of the subcutaneous lipoma in order to avoid creation of a large dead space. This is attributed to frequent inability to achieve primary closure of dura and necessaryuseofduralgrafts. Never remove the large subcutaneous lipoma at the time of intraspinal surgery due to higher likelihood of post-operative incision complication. In cases with large defects of the lumbodorsal fascia, the paramedian lumbodorsal fascia may be incised to create relaxing incisions and facilitate a sliding midline closure. Many studies suggest that earlier treatment prior to symptom development yields better prognosis. Retethering rates are relatively high, and maximal safe resection of the lipomatous malformation should be the goal to minimize the risk of retethering. Outcome of untethering for symomatic spina bifida occulta with lumbosacral spinal cord tethering in 31 patients: analysis of preoperative prognostic factors. Analysis of 153 patients with myelomeningocele or spinal lipoma reoperated upon for a tethered cord. She states that the opening has been present since birth and has not changed in appearance, drained, or exhibited signs of inflammation. She was born at full term via a normal delivery, after routine pre-natal care and an unremarkable pregnancy. Development has been normal, including rolling front to back and back to front, head elevation while prone, feeding, and social engagement. Detailed neurological examination by the neurosurgeon is unremarkable, with normal tickle response, reflexes, muscle bulk and tone, and symmetric spontaneous movements in both lower extremities. The palate is visibly and palpably normal as is the external examination of the midline from the nasal tip to the coccyx, with the exception of the noted lumbar opening. Assessment and Planning the pediatric neurosurgeon suspects the presence of a dermal sinus tract. The differential diagnosis includes a benign sacral dimple, or a dysraphic sacral dimple suggestive of underlying closed dysraphism (typically a thickened filum terminale or other fatty malformation of the distal cord and/or filum). Although the exact incidences of these entities are not well defined, in general benign dimples are extremely common, dysraphic dimples rare, and dermal sinus tracts extremely rare. A punctate opening is seen a few millimeters left of midline, just above the top of the gluteal fold, representing the superficial presentation of a dermal sinus tract. Despite their rarity, concern about the presence of a dermal sinus tract drives referral for imaging and pediatric neurosurgery evaluation in many cases. This is because, in addition to the gradual and subtler loss of function typically encountered with minor closed dysraphism (often a fatty and thickened filum terminale causing tethered spinal cord), children with dermal sinus tracts (extremely rarely) present with fulminant pyogenic infection of the conus medullaris or cauda equina resulting in permanent, serious loss of function, including paralysis. Physical examination is crucial to the accurate diagnosis of lumbosacral pits and dimples. True coccygeal dimples are generally round and smooth edged, 3 to 4 mm in diameter, and are positioned over the sharp tip of the coccyx on palpation. Although there is an intact skin plane at the bottom of a true sacrococcygeal dimple, it can be hard to see. Dimples over the back of the sacrum may be associated with a thickened and fatty filum terminale or other closed dysraphism. They may also be associated with a deviation or Y-shape of the upper gluteal fold. Pits are much more focal and punctate than dimples, often having a "punched out" appearance. A true pit may contain one or two dark or dysplastic hairs and may have a small surrounding or satellite 48 Spinal Dermal Sinus Tract 2. Palpation may reveal underlying areas of firm or rubbery dermoid material and there may rarely be inflammatory signs. It is critical to inspect the entire midline integument, from the nasal tip to the distal sacrum. Children presenting with repeated bouts of confirmed bacterial meningitis, often with variable skin flora, should undergo a meticulous examination of the dorsal midline, oropharynx, and nasal palate, looking for potential dermal sinus tracts or basal encephaloceles as a point of entry. Contrary to standard teaching, dermal sinus tracts may occasionally occur within the upper midline gluteal fold (over the proximal sacrum but not the coccyx). Conversely, the majority of dimples appearing cranial to the fold do not represent dermal sinus tracts, but may be associated with closed dysraphism, such as a thickened filum terminale. It is extremely important to correlate the physical examination, including the exact dorsal level of the pit or tract, with the imaging (ideally with a superficial vitamin E skin marker). A tract in the superficial soft tissues over the spine in most cases can be tracked on sagittal images all the way to insertion on the dorsal aspect of the conus medullaris just cranial to insertion of the filum terminale. There is often a "beads on a chain"appearance of focal areas of thickening in the dermal sinus tract where accumulation of dermoid material in the tract is more prominent.

These are sufficient to supply 6 to 8 cm of small intestine if the adjacent vasa recta have been occluded or ligated anxiety breathing problems 10 mg buspirone buy free shipping. The unpaired inferior mesenteric artery branches off the abdominal aorta approximately 5 cm above its bifurcation and turns to the left side anxiety symptoms treatment and prevention 10 mg buspirone buy otc. With the exception of a short terminal section anxiety level test 10 mg buspirone with visa, the inferior mesenteric artery descends into the retroperitoneal space to supply the descending colon and the upper rectum anxiety images order buspirone 10 mg without a prescription. Left colic artery: ascends along the descending colon and anastomoses via the left colic artery with the middle colic artery from the superior mesenteric artery (Riolan anastomosis) anxietyzone symptoms poll cheap buspirone 10 mg on-line. Superior rectal artery: supplies rectum and the rectal cavernous bodies in the submucosa (corpus cavernosum of rectum), which are a part of the continence mechanism. Ventral view; after opening of the mesentery with the transverse colon reflected cranially. Within the mesentery, the superior mesenteric artery gives rise to the following branches: jejunal arteries and ileal arteries to the left side and middle colic artery, right colic artery, and ileocolic artery to the right side. At the left colic flexure, the middle colic artery forms a functionally important anastomosis (Riolan anastomosis) with the left colic artery from the inferior mesenteric artery. This facilitates the formation of collateral circulations in the case of occlusion of one of the arteries. The anastomosis between the two arteries in one of the arcades close to the intestines is occasionally referred to as Drummond anastomosis. In the clinical jargon, all anastomoses in the area of the left colic flexure are summarized as Riolan anastomosis. The marginal artery gives rise to the vasa recta, which enter the colon wall and form intramural anastomoses. These intramural anastomoses are not as extensive as in the small bowel, and they can supply only 2 to 3 cm of colon compared with the 6 to 8 cm in the small intestine. In approximately 5% of patients, the marginal artery is deficient in one or more of the following areas: the last 6 to 8 cm of the terminal ileum, between the ileocolic and right colic arteries, between the middle and left colic arteries (termed the avascular area of Riolan), and between the superior rectal and last sigmoid arteries. The surgeon should be aware of these deficiencies because they may lead to compromise of intestinal integrity. Identification of the major arteries before resection of a portion of the colon can help avoid the unfavorable situation of unrecognized vascular insufficiency. Ventral view; transverse colon reflected cranially and small intestinal loops to the right side. Following its origin above the aortic bifurcation, the inferior mesenteric artery descends in the retroperitoneal space and releases first the left colic artery to the left side, then several sigmoid arteries, and finally the unpaired superior rectal artery. The left colic artery ascends along the descending colon, forms arcades, and anastomoses with the middle colic artery derived from the superior mesenteric artery (Riolan anastomosis). The anastomosis between the two arteries in one of the arcades close to the intestines is occasionally referred to as the Drummond anastomosis. The collateral mesenteric communications are important in the setting of occlusive disease. The portal vein ascends to the liver behind the bile duct and hepatic artery at the free edge of the lesser omentum. At the porta hepatis, the portal vein divides into the left and right branches, which eventually empty into the hepatic sinusoids. The portal system does have several anastomoses with the systemic venous system, which can compensate for obstructed portal venous return. The lymphatic system of the colon also follows the arterial supply previously described. Intramural lymphatic channels drain into extramural lymph vessels, which empty into the colonic lymph nodes. Anatomy of the Small Intestine the small intestine extends from the pylorus to the cecum and consists of the duodenum, jejunum, and ileum. Rectum and anal canal are supplied by three arteries: superior rectal artery (unpaired), from the inferior mesenteric artery; middle rectal artery (paired): from the internal iliac artery above the pelvic floor (levator ani); inferior rectal artery (paired), from the internal pudendal artery beneath the pelvic floor. The border between the corresponding arterial supply from the inferior mesenteric artery and the internal iliac artery is located at the pectinate line, where numerous anastomoses between these arteries exist. The superior rectal artery is the last branch of the inferior mesenteric artery and provides a branch for the anastomosis with the sigmoid arteries. From this point onward (clinical term, Sudeck point [*]), the superior rectal artery (clinical term, superior hemorrhoidal artery) is considered a terminal artery. The corpus cavernosum of rectum is primarily supplied by the superior rectal artery. Therefore, bleeding of hemorrhoids, which represent dilated rectal cavernous bodies, is arterial bleeding, as shown by the bright red color. In addition, the small intestine contributes to the immune system and endocrine system. Together, the jejunum and ileum measure approximately 6 to 7 m in length, with the jejunum comprising the proximal 40% and the ileum accounting for the distal 60%. Despite the fact that there is no sharp morphologic distinction between the jejunum and ileum, there are certain characteristics that help distinguish between the two: 1. The jejunum has a thicker wall owing to the fact that the circular folds, or plicae circulares, are larger and well developed in the proximal end of the small bowel; these folds are small in the superior part of the ileum and absent in the terminal ileum. Of these, the free taenia is visible, whereas the mesocolic taenia attaches to the transverse mesocolon and the omental taenia connects to the greater omentum. The haustra are sacculations of the intestinal wall that correspond to crescent-shaped mucosal folds (plicae semilunares) at the inner surface. Finally, the large intestine has epiploic appendices: fatty projections from the adipose tissue of the subserosa. The jejunal mesentery contains less fat than that of the ileum, and the arterial arcades are easier to visualize than in the ileum. The jejunum has fewer arterial arcades with longer vasa recti compared with the ileum. These infoldings correspond to transverse folds in the bowel lumen called plicae semilunares. The large bowel has three thickened bands of longitudinal muscle that run its length from the appendix to the rectum called taeniae coli (taenia omentalis, taenia libera, and taenia mesocolica). The large bowel has small pouches of peritoneum filled with fat called appendices epiploicae that are most prominent on the descending and sigmoid colon. It is a blind pouch that is 5 to 7 cm in length and projects caudal to the ileocecal junction in the right iliac fossa of the right lower quadrant. Usually, the cecum is entirely enveloped by peritoneum but does not have a mesentery. It is the widest part of the large intestine but also has the thinnest wall; thus, it is at highest risk for perforation in cases of large bowel obstruction. The appendix has its own short mesentery called the mesoappendix, which connects it to the inferior part of the mesentery of the ileum. The appendiceal artery is a branch off the ileocolic artery and runs in the mesoappendix. The ascending colon measures approximately 15 to 20 cm long and runs from the ileocecal valve to the hepatic flexure. It ascends as a retroperitoneal structure covered by peritoneum only on its anterior and lateral surfaces. It lies anterior to the quadratus lumborum, psoas, and transversus abdominis muscles; inferior pole of the right kidney; and descending portion of the duodenum. Lateral to the ascending colon is the white line of Toldt, which represents the fusion of the colonic mesentery with the parietal peritoneum. There may be congenital adhesions between the anterior aspect of the ascending colon and the right abdominal wall (Jackson membrane). The ascending colon and hepatic flexure are supplied by the ileocolic and right colic arteries, and the venous drainage is through the ileocolic and right colic veins, which drain into the superior mesenteric vein. The lymphatic drainage of the ascending colon is via the paracolic and epicolic lymph nodes, which empty into the superior mesenteric lymph nodes. The transverse colon is the portion of large bowel that lies between the hepatic and splenic flexures. It is the longest portion of the large bowel and usually measures 30 to 60 cm in length. Unlike the ascending and descending colon, the transverse colon has its own mesentery, which is longest in the center, and is therefore considered an intraperitoneal structure. The root of the mesentery of the transverse colon covers the descending part of the duodenum, the pancreas, and a portion of the left kidney. At the hepatic and splenic flexures, the mesentery is very short and may place the transverse colon in contact with the duodenum and the head of the pancreas, which may be injured during mobilization of the hepatic flexure. The splenic flexure is connected to the diaphragm by the phrenocolic ligament and to the spleen by the lienocolic ligament. The descending colon is approximately 20 to 25 cm in length; it begins at the splenic flexure and ends at the pelvic brim with the start of the sigmoid colon, which is demarcated by its intraperitoneal mesentery. The proximal part of the descending colon is attached to the peritoneum overlying the left kidney by the phrenicocolic ligament. Similar to the ascending colon, the descending colon is a retroperitoneal structure that is covered by peritoneum only on its anterior and lateral surfaces. Lateral to the descending colon is the white line of Toldt, which demarcates the correct plane to enter the retroperitoneal space to mobilize the descending colon. The sigmoid colon begins at the pelvic brim, curves inferiorly along the left pelvic side wall over the bifurcation of the left common iliac artery, and finally runs in the midline. The sigmoid mesocolon begins at the pelvic brim and becomes longer to the midpoint of the sigmoid colon and then decreases in size as it travels inferiorly. The sigmoid colon becomes the rectum in front of the sacrum at the level at which the sigmoid colon mesentery ends and the appendices epiploicae disappear. The taeniae coli become more diffuse around the rectum and form a complete outer layer of longitudinal muscle. The longitudinal muscles merge with the perineal body and with muscles of the external sphincter. Proximally it is of similar diameter as the sigmoid colon, but more distally it widens to the infraperitoneal ampulla, which is capable of significant distention. The upper third of the rectum is covered by peritoneum anteriorly and laterally, the middle third is covered only anteriorly, and the lower third is without peritoneal covering. The peritoneum is tented forward to the upper vagina to form the rectouterine pouch of Douglas. The rectum passes inferiorly through a ligamentous gate formed by the left and right ligamentum sacrouterinum and travels posterior to the vagina. This surgical plane between the posterior vagina and the rectum is an important landmark during surgical procedures for gynecologic cancer because here the retroperitoneum can be entered below the peritoneal reflection and the perirectal fat and the anterior rectum can be developed in preparation for the resection. Surgical Techniques General Principles of Intestinal Surgery Avoiding tissue trauma, gaining adequate exposure, and using knowledge of anatomy are essential in the performance of any surgical procedure, and especially with intestinal surgery. Selection of instruments, positioning, suture material, and stapling techniques are important but not as essential as the manner in which the details are executed. In addition, there are several important principles of successful intestinal surgery: 1. Chapter 17 Small Bowel and Large Bowel Resection and Anastomosis 235 Maintain an adequate lumen. Consider a diverting ostomy in the setting of infection, peritonitis, or radiation changes. Intestinal Anastomosis Techniques of Bowel Anastomosis Intestinal anastomoses can be performed using one of two general techniques: hand-sewn or stapled. Although the introduction of intestinal staplers has simplified and accelerated the creation of a bowel anastomosis, there are times when the hand-sewn technique may be indicated or useful, and the surgeon should be familiar with both techniques. Independent of the technique used, there are several general principles that are necessary to ensure a successful anastomosis. Hand-Sewn Anastomoses Hand-sewn anastomosis can be divided into two categories: one-layer and two-layer anastomoses. Variations in technique exist, including interrupted versus continuous closure, and the selection of absorbable or permanent suture. The small intestine heals very rapidly, reaching maximal strength in approximately 14 to 21 days. This rate of colonic healing is similar to the rapid rate of healing of the small intestine. The antimesenteric edge is farthest away from the blood supply and is at highest risk for underperfusion. The traditional hand-sewn small bowel anastomosis is performed by using a one-layer or a two-layer inverting technique. The sequence of layer closure depends on the mobility of the portions of intestine to be anastomosed. The bowel ends are approximated with bowel clamps and two stay sutures, incorporating the seromuscular layer, placed midway between the mesenteric and antimesenteric borders to aid in alignment. The two-layered anastomosis begins with a placement of a single row of imbricating (Lembert) sutures on the posterior wall through the seromuscular layer. This is accomplished by using a continuous running suture on the posterior mucosal edges and a Connell inverting suture on the anterior mucosal edge. The anastomosis is then completed by placing a row of imbricating (Lembert) sutures on the anterior wall, placing all the sutures before tying them. The one-layer closure has the advantage of decreasing the time required to form the anastomosis and producing a wider lumen because less of the bowel edge is inverted. Full-thickness sutures should be placed 5 mm from the edge (out to in), and ideally 1 to 2 mm of mucosa (for hemostasis) should be incorporated on both ends before exiting 5 mm from the edge on the contralateral side (in to out). The bowel is turned 180 degrees, and a second mesenteric suture is placed right next to the previous one and tied as described earlier; then the suture is run to the antimesenteric side, where both sutures are tied together. The anastomosis is inspected, and interrupted sutures can be placed if necessary to ensure a watertight anastomosis.

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Diseases

• Lopes Gorlin syndrome
• Larsen syndrome
• Goldenhar syndrome
• Osteomalacia
• Treponema infection
• Deafness, X linked, DFN

References

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