By P. Brenton. Southern Oregon University.
Mesenteric ischemia was associated with both early and late mortality in a single-center buy nicotinell 52.5mg with visa, retrospective study of 543 patients over 6 years buy nicotinell with paypal, causing 6 buy nicotinell 35mg with visa. Diagnoses included severe acute pancreatitis, intestinal or gastric perforation, bowel obstruction, and biliary infection, all of which were associated with high hospital mortality (33. Beyond typical historical elements (onset, quality, severity, location, radiation, exacerbating and alleviating symptoms), additional information about constitutional symptoms, gastrointestinal, and gynecologic symptoms should be obtained. Special attention should be paid to prior medical and surgery history, medications, and social history. However, the information obtained from the patient may be used to identify risk factors for particular intraabdominal processes (see Table 51. Long regarded an essential part of the abdominal examination, auscultation is neither specific nor sensitive . Patients with focal pain or obstructive symptoms should be carefully examined for evidence of inguinal or incisional hernias. Comorbid conditions such as diabetes and chronic immunosuppression may blunt examination findings associated with intraabdominal pathologies. Diagnostic imaging provides critical clinical data during the evaluation, particularly when physical examination findings are unreliable secondary to sedation, obtundation, delirium, or immunosuppression. Plain Radiographs Abdominal radiographs are rapidly and widely available, inexpensive studies that are frequently obtained for patients with abdominal pain. After an intraabdominal exploration or procedure, free air should not persist for more than 48 to 72 hours. Contrast- enhanced X-rays can be used to confirm the placement of gastrostomy and jejunostomy tubes, or to evaluate bowel motility. Ultrasound Ultrasound offers distinct advantages for evaluating abdominal pathologies of the critically ill care. Bedside ultrasound can be used to assess a variety of acute findings, including free fluid, pneumothorax, pericardial effusions, gallbladder disease, aortic aneurysm, intrauterine pregnancy, hydronephrosis, bladder volume, and inferior vena cava diameter (as a marker of volume resuscitation). There are several settings in which technical limitations to ultrasound arise, including morbid obesity and the presence of bowel gas. Acute mesenteric ischemia and acalculous cholecystitis are discussed in detail here, as these are common reasons for surgical consultation for critically ill adults. Abdominal compartment syndrome, surgical infections, and necrotizing fasciitis (Fournier’s gangrene) are separately covered within this section. Acute Mesenteric Ischemia Acute mesenteric ischemia can be a difficult diagnosis to make, and clinicians must maintain a high degree of suspicion particularly for elderly patients with severe abdominal pain. With bacterial translocation occurring 6 hours after disruption of ischemic mucosal barrier, correcting the subsequent physiologic insults is challenging, because the diagnosis takes an average of 8 hours and treatment can take another 2. Even with prompt initiation of anticoagulation for thromboembolic events with intravenous heparin (5,000 International Units bolus followed by 20,000 International Units over 24 hours), morbidity and mortality are substantial. Among patients for whom the diagnosis is delayed by 24 hours, mortality nearly doubles from 36% to 69% . Cholecystitis Acalculous cholecystitis is more frequent among the critically ill than typical stone-based disease. Acalculous cholecystitis reflects ischemic or inflammatory changes to the gallbladder secondary to obstruction of the cystic duct, bile stasis, or distention . Acute acalculous cholecystitis is frequently diagnosed among patients with an admission diagnosis of sepsis . The most common modality for the evaluation of acalculous cholecystitis is ultrasound; however, the absence of stones can decrease the sensitivity of this test . Definitive therapy with open or laparoscopic cholecystectomy is associated with increased perioperative mortality among critically ill patients, leading to alternatives (percutaneous cholecystostomy tube placement) . A retrospective observational study of 56 patients treated for acalculous cholecystitis with percutaneous cholecystostomy demonstrated an efficacy of over 80%, with low rates of associated complications, mortality, or need for subsequent cholecystectomy . Often representing a further progression of multisystem organ failure, acute acalculous cholecystitis requires prompt intervention with low-risk surgical interventions available that can accommodate patients unfit for anesthesia or transport . Clinicians must remain vigilant for extraabdominal sources of pain, particularly when abdominal imaging is unremarkable or equivocal. Impaired or dwindling physiologic reserves exacerbate failing organ systems and potentiate comorbidities . Multidisciplinary approaches involving palliative care teams, geriatricians, primary care physicians, as well as the surgeon and intensivist, enable the identification of cases where a comfort-oriented care plan is appropriate. The Surviving Sepsis Campaign: International Guidelines for Management of Severe Sepsis and Septic Shock, 2012, summarizes evidence-supported early interventions for the septic patient by international consensus and are appropriate for the critically ill patient with abdominal sepsis. Recommendations include quantitative resuscitation with appropriate reevaluation of end points, acquisition of blood cultures prior to initiation of broad-spectrum antibiotics, prompt acquirement of ancillary imaging, and source control by appropriate modality (with consideration of risks and benefits) within 12 hours. Hemodynamic lability in such circumstances may prevent patient transport, increasing the burden on the clinician to work with physical examination, and available laboratory, and ancillary bedside diagnostics. High clinical suspicion of intraabdominal sepsis in these circumstances warrants exploratory laparotomy and its associated high mortality and morbidity . When associated with hypothermia, acidosis, and coagulopathy, the mortality risk becomes nearly prohibitive. Wide surgical source control of devitalized tissues, perforated viscus, or anastomotic failures remain a priority to reduce both bacterial load and source . Bowel edema secondary to resuscitation, ongoing or unresolved contamination from perforated or compromises viscous, and clear anticipation of abdominal compartment syndrome may warrant leaving the abdomen open with placement of a negative pressure wound therapy device . Open abdomens in the non-trauma patient have become more widely described in recent years with concerns noted for high mortality and enterocutaneous fistula formation, but with the caveat that many of these scenarios are predisposed to both outcomes as expected sequelae of inflamed, swollen bowel and severe sepsis [23,24]. There exists substantial heterogeneity regarding the indications for the open abdomen among critically ill patients, whether deliberate or unavoidable. While initial maneuvers performed during source control (damage control) surgery require debridement of devitalized tissues, removal of infected foreign bodies, irrigation and drainage of contaminated surfaces, and abdominal decompression, the subsequent restoration of anatomic function is less of an immediate priority . An emerging literature has embraced delayed reconstruction of bowel continuity, with some indication that resuscitation and optimization of anastomosis creation may lead to improved survival and fewer complications . Impediments to the pragmatic approach and treatment of the acute abdomen include patient complexity, poor clinical correlates, and delays in diagnosis secondary to confounding from coexisting ailments. A multidisciplinary approach designed to maximize utilization of physical examination findings, laboratory results, imaging modalities, and collaborative clinical judgment results in the best opportunity for early intervention and improved outcomes. Zhou J, Qian C, Zhao M, et al: Epidemiology and outcome of severe sepsis and septic shock in intensive care units in mainland China. Cheng B, Xie G, Yao S, et al: Epidemiology of severe sepsis in critically ill surgical patients in ten university hospitals in China. De Waele J, Lipman J, Sakr Y, et al: Abdominal infections in the intensive care unit: characteristics, treatment and determinants of outcome. Felder S, Margel D, Murrell Z, et al: Usefulness of bowel sound auscultation: a prospective evaluation. Treinen C, Lomelin D, Krause C, et al: Acute acalculous cholecystitis in the critically ill: risk factors and surgical strategies. Hecker A, Uhle F, Schwandner T, et al: Diagnostics, therapy and outcome prediction in abdominal sepsis: current standards and future perspectives. This secondary form is caused by severe systemic illness and the resultant capillary leak and typically is related to large volume resuscitation .
Their functions vary depending on the tissue and the specific enzymes within the pathway that are available at that particular site 52.5 mg nicotinell fast delivery. The net effect on platelets and blood vessels depends on the balance of these two prostanoids order generic nicotinell line. Therapeutic uses of prostaglandins Prostaglandins have a major role in modulating pain best nicotinell 35 mg, inflammation, and fever. Prostaglandins are among the chemical mediators released in allergic and inflammatory processes. The ductus closes soon after delivery to allow normal blood circulation between the lungs and the heart. In neonates with congenital heart conditions, infusion of alprostadil keeps the ductus open, allowing time until surgical correction is possible. It stimulates chloride channels in the luminal cells of the intestinal epithelium, thereby increasing intestinal fluid secretion (see Chapter 40). Nausea and diarrhea are the most common adverse effects of lubiprostone (ure 38. Misoprostol interacts with prostaglandin receptors on parietal cells within the stomach, reducing gastric acid secretion. Its use is limited by common adverse effects including diarrhea and abdominal pain. By binding to prostaglandin receptors, they increase uveoscleral outflow, reducing intraocular pressure. They are administered as ophthalmic solutions once a day and are as effective as timolol or better in reducing intraocular pressure. Bimatoprost increases eyelash prominence, length, and darkness and is approved for the treatment of eyelash hypotrichosis. Ocular reactions include blurred vision, iris color change (increased brown pigmentation), increased number and pigment of eyelashes, ocular irritation, and foreign body sensation. These drugs mimic the effects of prostacyclin in endothelial cells, producing a significant reduction in pulmonary arterial resistance with a subsequent increase in cardiac index and oxygen delivery. Epoprostenol and treprostinil are administered as a continuous intravenous infusion, and treprostinil is administered orally or via inhalation or subcutaneous infusion. Dizziness, headache, flushing, and fainting are the most common adverse effects (ure 38. They act primarily by inhibiting the cyclooxygenase enzymes that catalyze the first step in prostanoid biosynthesis. This leads to decreased prostaglandin synthesis with both beneficial and unwanted effects. Mechanism of action Aspirin is a weak organic acid that irreversibly acetylates and, thus, inactivates cyclooxygenase (ure 38. Anti-inflammatory actions Inhibition of cyclooxygenase diminishes the formation of prostaglandins and, thus, modulates aspects of inflammation mediated by prostaglandins. One exception is ketorolac, which can be used for more severe pain, but for only a short duration. Antipyretic action Fever occurs when the set-point of the anterior hypothalamic thermoregulatory center is elevated. This rapidly lowers the body temperature of febrile patients by increasing heat dissipation through peripheral vasodilation and sweating. For example, two 325-mg aspirin tablets administered four times daily produce analgesia, whereas 12 to 20 tablets per day produce both analgesic and anti-inflammatory activity. Chronic use of aspirin allows for continued inhibition as new platelets are generated. External applications Salicylic acid is used topically to treat acne, corns, calluses, and warts. Methyl salicylate (“oil of wintergreen”) is used externally as a cutaneous counterirritant in liniments, such as arthritis creams and sports rubs. Diclofenac is available in topical formulations (gel or solution) for treatment of osteoarthritis in the knees or hands. In addition, ocular formulations of ketorolac are approved for management of seasonal allergic conjunctivitis and inflammation and pain related to ocular surgery. Aspirin After oral administration, aspirin is rapidly deacetylated by esterases in the body to produce salicylate. Unionized salicylates are passively absorbed mainly from the upper small intestine. Salicylates (except for diflunisal) cross both the blood–brain barrier and the placenta and are absorbed through intact skin (especially methyl salicylate). Salicylate is converted by the liver to water-soluble conjugates that are rapidly cleared by the kidney, resulting in first-order elimination and a serum half-life of 3. At anti-inflammatory dosages of aspirin (more than 4 g/day), the hepatic metabolic pathway becomes saturated, and zero-order kinetics are observed, leading to a half-life of 15 hours or more (ure 38. Therefore, aspirin should be avoided in gout, if possible, or in patients taking probenecid. Platelet aggregation is the first step in thrombus formation, and the antiplatelet effect of aspirin results in a prolonged bleeding time. Decreased synthesis of prostaglandins can result in retention of sodium and water and may cause edema. Patients with a history of heart failure or kidney disease are at particularly high risk. These effects can also mitigate the beneficial effects of antihypertensive medications. Approximately 15% of patients taking aspirin experience hypersensitivity reactions. Drug interactions Salicylate is roughly 80% to 90% plasma protein bound (albumin) and can be displaced from protein-binding sites, resulting in increased concentration of free salicylate. Alternatively, aspirin can displace other highly protein-bound drugs, such as warfarin, phenytoin, or valproic acid, resulting in higher free concentrations of these agents (ure 38. Toxicity Mild salicylate toxicity is called salicylism and is characterized by nausea, vomiting, marked hyperventilation, headache, mental confusion, dizziness, and tinnitus (ringing or roaring in the ears). When large doses of salicylate are administered, severe salicylate intoxication may result (see ure 38. Restlessness, delirium, hallucinations, convulsions, coma, respiratory and metabolic acidosis, and death from respiratory failure may occur. Children are particularly prone to salicylate intoxication; ingestion of as little as 10 g of aspirin can be fatal. The dosage should be reduced in those with moderate hepatic impairment, and celecoxib should be avoided in patients with severe hepatic or renal disease. Adverse effects Headache, dyspepsia, diarrhea, and abdominal pain are the most common adverse effects.
A finger is inserted into the pleural space to explore the anatomy and confirm proper location and lack of pleural symphysis discount nicotinell american express. The end of the chest tube is grasped with the clamp and guided with the finger through the tunnel into the pleural space generic nicotinell 17.5mg online. Once the tip of the tube is in the pleural space order nicotinell 17.5mg mastercard, the clamp is removed, and the chest tube is advanced and positioned apically for a pneumothorax and dependently for fluid removal. The location of the tube should be confirmed by observing the flow of air (seen as condensation within the tube) or fluid from the tube. A simple suture to anchor the tube can be used, or a horizontal mattress suture can be used to allow the hole to be tied closed when the tube is removed. An occlusive petrolatum gauze dressing is applied, and the tube is connected to a drainage apparatus and securely taped to the dressing and to the patient. The end of the chest tube is grasped with a Kelly clamp and guided with a finger through the chest incision. In one series, insertion and management of pleural tubes in patients with blunt chest trauma carried a 9% incidence of complications. Major complications requiring surgical intervention, or administration of blood products or intravenous antibiotics occurred in only four (1. The use of small-caliber, less rigid, Silastic drains has been found to be as safe and efficacious as the more rigid, conventional chest tubes . Most institutions use a three-chambered system that contains a calibrated collection trap for fluid; an underwater seal unit to allow escape of air while maintaining negative pleural pressure; and a suction regulator. Suction is routinely established at 15 to 20 cm water, controlled by the height of the column in the suction regulator unit, and maintained as long as an air leak is present. The drainage system is examined daily to ensure that appropriate levels are maintained in the underwater seal and suction regulator chambers. Connections between the chest tube and the drainage system should be tightly fitted and securely taped. For continuous drainage, the chest tube and the drainage system tubing should remain free of kinks; should not be left in a dependent position; and should never be clamped. Routine milking and stripping of chest tubes is discouraged primarily in postoperative cardiac surgical patients. Dressing changes should be performed every 2 or 3 days and as needed, making sure that no dressing with high content of petroleum-based ointment is present, because this would macerate the skin around the chest tube insertion site. Adequate pain control is mandatory to encourage coughing and ambulation to facilitate lung reexpansion. If the patient develops clinical symptoms including shortness of breath, decreasing oxygen saturation, or subcutaneous emphysema, then radiographic evaluation is indicated . A tube should never be readvanced into the pleural space, and if a tube is to be replaced, it should always be at a different site. If an air leak persists, brief clamping of the chest tube can be performed to confirm that the leak is from the patient and not from the system. When the leak has ceased for more than 24 to 48 hours (or if no fluctuation is seen in the underwater seal chamber), the drainage system is placed on water seal by disconnecting the wall suction, followed by a chest film several hours later. If no pneumothorax is present and no air leak appears in the system with coughing; deep breathing; and reestablishment of suction, the tube can be removed. For fluid collections, the tube can be removed when drainage is less than 200 mL per 24 hours , unless sclerotherapy is planned. When the chest tube is removed, the lungs should be fully expanded, which minimizes the pleural space. This can only be achieved when the patient holds his/her breath while performing the Valsalva maneuver (i. Variation of success rates could be affected by a number of reasons including the underlying disease, the use of mechanical ventilation, or other factors . Also, there have been reports of successful management of small and large pneumothoraces with small size (8. Thirty-six (60%) patients were discharged after 4 hours, and 30 patients (50%) were managed as outpatients. Because evacuation of a pneumothorax and removal of pleural fluid are the main indications for chest tube insertion, ultrasonography has application for chest tube insertion and care. The linear high frequency probe lacks sufficient penetration to visualize deeper thoracic structures such as atelectatic lung underlying the pleural effusion, but is useful for identification of lung point while mapping out the extent of a pneumothorax. A free-flowing pleural effusion will assume a dependent position in the thorax owing to gravitational effect, so the operator examines for fluid over the lateral chest in the supine patient. The operator can readily locate a loculated effusion and insert a targeted chest tube for drainage of the pleural fluid . Chest Tube Insertion and Care Ultrasonography permits selection of a chest tube with the appropriate and safe angle and depth for insertion into a pleural effusion. The principles of site selection for chest tube insertion are the same as for thoracentesis (see Chapter 12 Thoracentesis). Site selection can be done rapidly in the emergency situation (thoracic trauma, tension pneumothorax on ventilatory support). Unintentional insertion of the chest tube in a subdiaphragmatic position with injury to the liver or spleen, cardiac perforation, or lung insertion are all recognized complications of chest tube insertion that can be avoided by the simple expedient of using ultrasonography for all chest tube insertions, if the capability is available . Owing to the simplicity of the examination, ultrasonography is used to assess the amount of residual fluid. On occasion, a chest tube will not adequately drain the pleural effusion because of misplacement, tube blockage, or loculations. Ultrasonography can detect the adequacy of drainage; and, if the fluid is not being removed, guide decisions related to chest tube replacement or manipulation. Follow-up ultrasonography examinations take little time and are performed by the intensivist team at point of care as often as required in order to guide ongoing management of the chest tube. It is feasible to use ultrasonography as the main imaging modality for management of pleural fluid removal. Pneumothorax Scanning Technique A series of scan lines are performed over the chest in order to locate the pneumothorax and to establish a safe site for chest tube insertion that avoids injury to adjacent organs. In the supine patient, air in the pleural space will distribute anteriorly; so the examination for pneumothorax is concentrated over the anterior and lateral chest. Chest Tube Insertion and Care the presence of lung sliding, lung pulse, or B lines rules out pneumothorax at the site of the examination (See Chapter 11 Lung Ultrasonography). Multiple intercostal spaces can be examined in a short period time in order to exclude pneumothorax with a high level of certainty in the patient. Identification of a lung point verifies the presence of pneumothorax  and allows the operator to map out the lateral extent of the pneumothorax. Insertion where lung is still inflated against the chest wall may result in placement of the chest tube into the lung. The operator inserts the device into the area of the chest that lacks lung sliding and that is demarcated laterally by the lung point. Once the tube is inserted, adequacy of lung inflation is determined by the return of lung sliding, lung pulse, and/or B lines. The timing of chest tube removal following chest tube insertion for pneumothorax is guided with ultrasonography as follows [29–31]: 1.
Therefore buy nicotinell 52.5mg with visa, a “loading dose” of drug is administered to achieve the desired plasma level rapidly purchase nicotinell australia, followed by a maintenance dose to maintain the steady state buy nicotinell 35 mg mastercard. Loading dose = (V ) × (desired steady-state plasma concentration)/Fd Disadvantages of loading doses include increased risk of drug toxicity and a longer time for the plasma concentration to fall if excess levels occur. Dose adjustment the amount of a drug administered for a given condition is estimated based on an “average patient. Knowledge of pharmacokinetic principles is useful in adjusting dosages to optimize 74 therapy for a given patient. Monitoring drug therapy and correlating it with clinical benefits provides another tool to individualize therapy. For drugs with a defined therapeutic range, drug concentrations are measured, and the dosage and frequency are adjusted to obtain the desired levels. When determining a dosage adjustment, V can be used to calculate the amountd of drug needed to achieve a desired plasma concentration. For example, assume a heart failure patient is not well controlled due to inadequate plasma levels of digoxin. Suppose the concentration of digoxin in the plasma is C and1 the desired target concentration is C, a higher concentration. The following calculation can be used to determine2 how much additional digoxin should be administered to bring the level from C to C. Which of the following routes of administration is the most desirable for administering the antidote for the drug overdose? The intravenous route of administration is the most desirable because it results in achievement of therapeutic plasma levels of the antidote rapidly. If administered orally, at which of the following sites ofa absorption will the drug be able to readily pass through the membrane? For weak bases, the nonionized form will permeate through the cell membrane readily. Because the patient is 70 kg, the apparentd volume of distribution in L/kg will be approximately 1 L/kg (70. Which of the following is likely to be observed with use of Drug X in this patient? Because the patient has a renal disorder, she may not be able to excrete the drug effectively. As the half-life is prolonged, the dosage must be reduced so the patient will not have serious toxic effects of Drug X. Which of the following is the most likely contributor to her myocardial infarction today? The half-life of the drug after administration by continuous intravenous infusion is 12 hours. Which of the following best approximates the time for the drug to reach steady state? Therefore, for this drug with a half- life of 12 hours, the approximate time to reach steady state will be 48 hours. For oral dosing, loading dose = [(V ) × (desired steady-state plasma concentration)/F]. If the desired plasma concentration of digoxin for optimal therapeutic activity in heart failure is 1. The additional dosage of digoxin needed to achieve the desired plasma concentration can be calculated using the equation V (C – C ). Most drugs exert effects, both beneficial and harmful, by interacting with specialized target macromolecules called receptors, which are present on or in the cell. The drug–receptor complex initiates alterations in biochemical and/or molecular activity of a cell by a process called signal transduction (ure 2. A drug is termed an “agonist” if it binds to a site on a receptor protein and activates it to initiate a series of reactions that ultimately result in a specific intracellular response. The drug–receptor complex Cells have many different types of receptors, each of which is specific for a particular agonist and produces a unique response. Cardiac cell membranes, for example, contain β-adrenergic receptors that bind and respond to epinephrine or norepinephrine. Cardiac cells also contain muscarinic receptors that bind and respond to acetylcholine. These two receptor populations dynamically interact to control the heart’s vital functions. The magnitude of the cellular response is proportional to the number of drug–receptor complexes. This concept is conceptually similar to the formation of complexes between enzyme and substrate and shares many common features, such as specificity of the receptor for a given agonist. Although much of this chapter centers on the interaction of drugs with specific receptors, it is important to know that not all drugs exert effects by interacting with a receptor. Antacids, for instance, chemically neutralize excess gastric acid, thereby reducing stomach upset. Receptor states Receptors exist in at least two states, inactive (R) and active (R*), that are in reversible equilibrium with one another, usually favoring the inactive state. Binding of agonists causes the equilibrium to shift from R to R* to produce a biologic effect. Antagonists are drugs that bind to the receptor but do not increase the fraction of R*, instead stabilizing the fraction of R. Some drugs (partial agonists) shift the equilibrium from R to R*, but the fraction of R* is less than that caused by an agonist. In summary, agonists, antagonists, and partial agonists are examples of molecules or ligands that bind to the activation site on the receptor and can affect the fraction of R*. Major receptor families A receptor is defined as any biologic molecule to which a drug binds and produces a measurable response. Thus, enzymes, nucleic acids, and structural proteins can act as receptors for drugs or endogenous agonists. However, the richest sources of receptors are membrane-bound proteins that transduce extracellular signals into intracellular responses. These receptors may be divided into four families: 1) ligand-gated ion channels, 2) G protein–coupled receptors, 3) enzyme-linked receptors, and 4) intracellular receptors (ure 2. Generally, hydrophilic ligands interact with receptors that are found on the cell surface (ure 2. In contrast, hydrophobic ligands enter cells through the lipid bilayers of the cell membrane to interact with receptors found inside cells (ure 2. Ligand binds to a domain of a transmembrane receptor, which is coupled to a G protein. Ligand binds to the extracellular domain of a receptor that activates a kinase enzyme. Lipid-soluble ligand diffuses across the membrane to interact with its intracellular receptor. Transmembrane ligand-gated ion channels the extracellular portion of ligand-gated ion channels contains the drug-binding site. This site regulates the opening of the pore through which ions can flow across cell membranes (ure 2.
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