Academic literature on the topic 'Hypotensiv peristaltik'

Background Perioperative fluid restriction might be beneficial in specific clinical settings. In this prospective, randomized and blinded study, we assessed whether peristaltic pneumatic compression of the legs can support restrictive fluid management strategies by reducing intraoperative fluid demand and improving hemodynamic stability. Methods Seventy patients scheduled for minor surgery were randomly assigned to receive either intraoperative peristaltic pneumatic compression or placebo compression. Both groups received fluid therapy according to a goal-directed protocol with a crystalloid base rate of 2 ml · kg⁻¹ · h⁻¹ and bolus infusions of 250 ml crystalloids triggered by hypotension, tachycardia, or high Pleth Variability Index. Results Patients treated with peristaltic pneumatic compression received less intravenous fluid: median (interquartile range) 286 (499) versus 921 (900) ml (P < 0.001), resulting in a median difference of 693 ml (95% CI, 495-922 ml) and a median difference of 8.4 ml/kg (95% CI, 5.3-11.5 ml; P < 0.001). After the anesthesia induction phase, median overall infusion rates were 12.2 (14.1) ml · kg⁻¹ · h⁻¹ in the control group and 1.9 (0.4) ml · kg⁻¹ · h⁻¹ in the pneumatic peristaltic compression group (P < 0.001). Among patients treated with pneumatic peristaltic compression, the median cumulative time of hypotension was shorter (0 [12.5] vs. 22.6 [22.8] min; P = 0.002), fewer hypotensive events were recorded (39 vs. 137; P = 0.001), and median lowest individual systolic pressure was higher (92 [8] vs. 85 [16] mmHg; P = 0.002). Conclusions This study demonstrates that peristaltic pneumatic compression of the legs significantly improves hemodynamic stability and reduces fluid demand during minor surgery.

Acute intraluminal acid perfusion induces esophageal shortening in humans and opossums. Lower esophageal sphincter (LES) hypotension and peristaltic dysfunction occur in patients and animal models of reflux esophagitis. This study examined whether similar shortening and motor dysfunction occur in anesthetized opossums after repeated esophageal acid exposure and whether this is associated with longitudinal muscle (LM) hyperresponsiveness. Manometry used before and after 3 consecutive days of 45-min perfusion with 100 mmol/l HCl or normal saline measured esophageal length and motor responses to induced swallows. LM electrical and mechanical responses were assessed using standard isometric tension and intracellular recording techniques. Compared with controls, repeated acid perfusion induced erosive esophagitis and significant esophageal shortening, associated with enhanced LM responses to carbachol, a significantly depolarized resting membrane potential, and abnormal spike patterns. LES resting pressure and swallow-induced peristalsis were unaffected. In this model of reflux esophagitis, marked persistent esophageal shortening and associated LM hyperresponsiveness occur before significant LES or peristaltic dysfunction, suggesting that esophageal shortening is the earliest motor disorder induced by acid injury.

Clinical history, questionnaire data and response to antisecretory therapy are insufficient to make a conclusive diagnosis of GERD in isolation, but are of value in determining need for further investigation. Conclusive evidence for reflux on oesophageal testing include advanced grade erosive oesophagitis (LA grades C and D), long-segment Barrett’s mucosa or peptic strictures on endoscopy or distal oesophageal acid exposure time (AET) >6% on ambulatory pH or pH-impedance monitoring. A normal endoscopy does not exclude GERD, but provides supportive evidence refuting GERD in conjunction with distal AET <4% and <40 reflux episodes on pH-impedance monitoring off proton pump inhibitors. Reflux-symptom association on ambulatory reflux monitoring provides supportive evidence for reflux triggered symptoms, and may predict a better treatment outcome when present. When endoscopy and pH or pH-impedance monitoring are inconclusive, adjunctive evidence from biopsy findings (histopathology scores, dilated intercellular spaces), motor evaluation (hypotensive lower oesophageal sphincter, hiatus hernia and oesophageal body hypomotility on high-resolution manometry) and novel impedance metrics (baseline impedance, postreflux swallow-induced peristaltic wave index) can add confidence for a GERD diagnosis; however, diagnosis cannot be based on these findings alone. An assessment of anatomy, motor function, reflux burden and symptomatic phenotype will therefore help direct management. Future GERD management strategies should focus on defining individual patient phenotypes based on the level of refluxate exposure, mechanism of reflux, efficacy of clearance, underlying anatomy of the oesophagogastric junction and psychometrics defining symptomatic presentations.

Development of the extreme form of hypothyroidism defined as myxedema is very rare. Acute symptoms and their management have been described in detail previously. However, not much attention has been devoted to therapeutic challenges that are faced in the recovery phase of the treatment, especially pertaining to the gastrointestinal system. The link between myxedema and the appearance of severe Clostridium difficile infection (CDI) has not been established so far. A 61-year-old woman with no significant medical record was admitted to hospital because of infected heel pressure and thyroid dysfunction. A week later, due to hypothermia, hypotension, and unconsciousness, she was transferred to the intensive care unit. The clinical picture and the results of laboratory tests confirmed diagnosis of myxedema. After the introduction of resuscitative measures and hormonal substitution, patient’s condition stabilized within 10 days. Due to concomitant sepsis, initially piperacillin/tazobactam and later cefuroxime were administered. After 20 days of antibiotic therapy, the patient developed CDI that was resistant to the routine mode of treatment. The clinical recovery was achieved only after a fecal microbiota transplantation procedure. The function of the digestive tract in myxedema is disturbed by gastric achlorydia and reduced peristalsis, which in turn can predispose the small intestine to overgrowth of bacteria. The use of antibiotics can additionally decrease the intestinal bacterial diversity, favoring the overgrowth of Clostridium difficile. The authors conclude that myxedema may increase the likelihood of a treatment-resistant form of CDI that requires the implementation of fecal microbiota transplantation.

Aim. The aim of the study is to analyze the regularities of changes in the basic indicators of esophageal pH-impedance monitoring and high-resolution manometry in patients with non-erosive reflux disease (NERD), erosive reflux disease (ERD) and Barrett’s esophagus (BE) in comparison with healthy individuals.Materials and methods. 69 patients were examined, including 19 patients with NERD, 16 patients with ERD, 14 patients with BE and 20 individuals comprising the control group (CG). The gender structure was as follows: 44 male and 25 female patients. The average age of the examined patients was 46 years. All patients underwent 24-hour esophageal pH-impedance monitoring and high resolution manometry.Results. According to the data of 24-hour pH-impedance monitoring, the total time in the esophagus with pH < 4 was 2.4 % in the control group, 9 % in the NERD group, 20.25 % in the ERD group and 23.5 % in the patients with BE (p < 0.05). The average number of acid refluxes was 22.5 in CG, 61 in the NERD group, 77 in the ERD group and 86 in patients with BE (p < 0.05). The time of chemical clearance was 1.7 minutes in CG, 2.2 minutes in the group of patients with NERD, 2.9 minutes in the ERD group and 3 minutes in the BE group (p < 0.05). The mean nocturnal baseline impedance was 2483.5 Ohm in CG, 1775.0 Ohm in the NERD group, 771.0 Ohm in the ERD group and 911.0 Ohm in the BE group (p < 0.05). The normal parameters of the esophagogastric junction (EGJ) structure and function according to the data of highresolution manometry were observed among 85 % of the control group, 63 % of patients with NERD, 25 % of patients with ERD and 36 % of BE group. The presence of hiatal hernia (HH) and/or hypotension of lower esophageal sphincter (LES) was observed in 15 % of patients from the CG, in 37 % of patients with NERD, in 75 % of patients with ERD and in 64 % of patients with BE. The normal parameters of the motor function of the esophagus were observed in CG (85 %), as well as in patients with NERD (79 %). In patients with ERB and BE, normal motor activity was noted in 25 % and 29 % of the cases, respectively. Disturbances of the motor function of the thoracic esophagus in CG were represented in 10 % of the cases by ineffective peristalsis and hypercontractility in the form of distal esophagospasm in 5 % of the cases. In the NERD group, 16 % of patients had ineffective peristalsis and 5 % of patients had hypercontractility in the form of a hypercontractile esophagus. In patients of ERD and BE groups, the disorders of the motor function of the thoracic esophagus were predominantly represented by ineffective peristalsis, in 75 % and 50 % of the patients, respectively. In addition, in the group of patients with BE, in 21 % of the cases, motor function disorders were observed in the form of absence of thoracic esophagus contractions.Conclusion. It is shown that such indicators as increased level of acid exposure, increased amount of acid reflux, slowed chemical clearance, lowered mean nocturnal baseline impedance, as well as disorders in the structure and function of the esophageal-gastric junction and motility of the thoracic esophagus are associated with the severity of GERD.

Introduction: Iloprost is a potent prostacyclin (PGI2) analogue that is effective in the treatment of peripheral arterial disease, vasculitis, pulmonary hypertension, and secondary Raynaud’s phenomenon. Intravenous infusions are generally administered with the aid of a peristaltic pump to reduce the risk of adverse reactions caused by unintentional increases in the infusion rate. This increases the cost of care in terms of equipment and personnel and may limit the use of this drug. Materials and methods: We retrospectively analyzed 18,432 iloprost infusions administered between 1999 and 2009 to 272 patients with systemic sclerosis (n = 253) and 19 with peripheral arterial disease (n = 19). All infusions were administered in the day hospital over 6 h with a normal IV set-up with a roller flow regulator. Flow rates were set to deliver iloprost at 1-2 ng/kg/min. Rates were verified by direct drop counts during the first 15-20 minutes of the infusion and at each subsequent check. Results: There were no adverse events that were fatal, life-threatening, or associated with prolongation of hospitalization and very few events requiring intensive care or continuous monitoring. The latter included 4 cases of tachycardia/arrhythmia (extrasystoles in most cases), 3 cases of hypotension (systolic pressure < 80 mmHg), and 2 cases of hypertension (BP > 170/100 mmHg). All other adverse reactions were mild, reversible, and similar to those seen with iloprost infusion with peristaltic pump. Only one patient had to be switched to another prostanoid (due to intolerance). Discussion: Iloprost infusion administered with a normal IV flow regulator appears to be as safe, well tolerated, and effective as traditional infusion with a peristaltic pump.

Abstract Introduction: Myxedemic coma is a life-threatening medical emergency. It needs to be treated emergently & carries very high mortality. It involves multi-organ failure at cellular level due to severe thyroid hormone deficiency. Most common clinical presentation involves CVS. With advancement in health care it is now uncommon to see myxedemic coma especially associated with GI Bleed. Here in we present an interesting case of GI bleed associated with myxedemic coma. Case: 84 years old male was discovered in home, minimally responsive. EMS intubated & brought him to ED with agonal respirations, hypotensive & unresponsive, He was admitted to ICU. Past medical history was significant for smoking & hypertension. Physical Exam was significant for dryness of skin, obtundation, hypothermia, tachypnea & BMI &gt;30. Initial Labs revealed anemia with Hemoglobin of 5.1mg/dL, Hematocrit 17.5%, Hyponatremia-134meq/L, Hyperkalemia-K+ levels 5.3meq/L, BUN-84mg/dL & creatinine-4.1mg/dL, His serum TSH levels were 352 mIU/ml with low free T4 and T3 levels at 0.15ng/dl and 1.99pg/ml, respectively. Stool was positive with Blood. IV fluids were given.GI was consulted. He underwent emergent upper GI endoscopy, which found the Dieulafoy’s lesion at cardiac end of stomach & treated with a combination of epinephrine injection, argon laser, & 3 hemo-clips. He had 6 PRBCs transfused. He was started on IV Thyroxine, Liothyronine and Hydrocortisone. His mental status improved, & hemoglobin remained relatively stable. Later on, he decided to move to palliative care & was discharged to hospice. Discussion: Myxedemic coma is a term generally used to denote most severe decompensated hypothyroidism. The typical progression is lethargy evolving into a stupor & eventually into a coma with respiratory failure and hypothermia. It can lead to volume depletion, hyponatremia, & AKI, which can worsen to ATN if prolonged ischemia remains.GI bleed is a rare manifestation of myxedemic coma. Pathophysiology of GI bleed in these patients involves mucosal edema & mucopolysaccharide infiltration. Also, myxedemic coma is associated with neurological changes resulting in slow peristalsis & GI atony. This coupled with coagulopathy associated with decompensated hypothyroidism results in increased risk of bleeding. Dieulfoy’s lesion are rare cause of GI bleed. Stress & ischemic changes are one of the inciting factors for these lesions. These lesions are more common in elderly males & are associated with severe systemic illness similar to our patient. Treatment is usually supportive with goal of identifying the lesions, stopping the bleed & aggressively managing myxedemic coma. We present an interesting case of GI bleed associated with myxedemic coma now relatively uncommon with advancement in healthcare. It provides an excellent learning opportunity for clinicians to consider while managing these patients.

Nedsatt motilitet i esophagus kan vara en orsak till dysphagi. Högupplöst esophagusmanometri (HRM) är "golden standard" för att utvärdera esophagus motilitet. Defekter av motiliteten kan ses som avbrott i den isobariska konturen (IBC). Det finns ett samband mellan avbrott och inkomplett bolus clearance. Referensvärdena för HRM är utformade för att patienten ska ligga ner och svälja under undersökningen. Kroppens läge påverkar esophagus och värdena för HRM ändras signifikant beroende på om patienten ligger ned eller sitter upp. Det pågår diskussioner kring om undersökningen borde innefatta sväljningar i både liggande och sittande position för att öka den diagnostiska säkerheten. Denna studie innefattade 12 stycken patienter som frivilligt genomgick 10 extra sväljningar sittande utöver de i liggande position. En jämförelse i antalet avbrott i IBC gjordes mellan sväljningarna sittandes och liggandes. Resultatet visade att 24 av 118 sväljningar liggande hade avbrott i IBC och 94 var utan avbrott. När patienterna satt upp hade 68 av 120 sväljningar avbrott i IBC och 52 sväljningar utan avbrott. Hypotesen bekräftades då det föreligger en signifikant skillnad i antalet avbrott mellan sittande och liggande position. Det förekom fler avbrott i sittande position och avbrotten blev också längre i sittande position. Fortsatta studier med större urval erfordras.
Reduced motility in the esophagus can be a cause of dysphagia. High-resolution esophagus manometry (HRM) is the golden standard for evaluating esophageal motility. Defects of the motility can be seen as disruptions in the isobaric contour (IBC). There is a correlation between disruptions and incomplete bolus clearance. The references for HRM are made for the patient to lie down and swallow for the examination. The position of the body affects the esophagus and the values for HRM changes significantly depending on whether the patients is lying down or sitting up. There are discussions about whether the procedure should include both supine and sitting position to increase diagnostic reliability. This study included 12 patients who voluntarily underwent 10 additional swallows sitting up in addition to the supine position. A comparison of the disruptions in IBC was made between the swallows sitting and supine. The results showed that 24 out of 118 supine swallows had disruptions in IBC and 94 were without. When the patients sat up, 68 out of 120 swallows had disruptions in IBC and 52 were without. The hypothesis was confirmed as there were more disruptions in the sitting position and the disruptions were longer. Further studies are required.

As with all acute patients, always start by assessing ABCDE: airways, breathing, circulation, disability, and exposure. In a patient with acute gastrointestinal (GI) haemorrhage (whether upper or lower), assessing their circulation (i.e. haemodynamic status) is a priority. If there are clinical features to suggest haemodynamic instability—such as hypotension, tachycardia, cool peripheries, tachypnoea, or decreased consciousness—then the immediate priority is to resuscitate the patient before proceeding to a thorough history and examination. The differential diagnosis for rectal bleeding is shown in Figure 21.1. There are a couple of points to note about this differential diagnosis. GI haemorrhage may present as overt or occult bleeding. This table, and the indications of prevalence within it, refers to overt rectal bleeding as occult rectal bleeding will not be noticed by the patient. The second point to note is that upper GI sources of haemorrhage may occasionally present with rectal bleeding alone. Although it is more likely that such upper GI sources will also present with haematemesis, you should note that large volumes of blood in the GI tract can act as a cathartic (stimulant of peristalsis) and the resultant rapid transit through the intestine leads to the passage of red blood per rectum. • How much blood has been passed? This question is directly relevant to your initial haemodynamic status survey. Ask the patient to quantify approximately how much blood they have passed—familiar measures such as a teaspoon, eggcup, or wine glass may be easier for the patient than asking them to provide an estimate in millilitres. Note, however, that it is very easy to overestimate volumes of blood loss if, for example, blood has mixed with water in the toilet bowl. You should additionally enquire about symptoms of hypovolaemia—any light-headedness, collapse, chest pain or breathlessness? • What is the duration and frequency of the symptoms? • What did the blood look like? Generally speaking, the fresher the blood, the more distal the bleed. Substantial bleeding from lesions proximal in the GI tract may present with melaena (jet black, tarry stool caused by bacterial oxidation of haem) or may present as frank blood (haematochezia) if transit times are sufficiently rapid.