Heartburn
Heartburn is a burning pain located behind the breastbone. Heartburn frequently associated with acid reflux is frequently induced by food especially fatty, sweet, spicy, chocolate, onions, citrus and tomato products. Lying down, bending, lifting and some exercises can trigger heartburn. Etiology of heartburn involves acid reflux non-acidic or weakly acidic reflux injury to the lining of the esophagus, bile acid, mechanical stimulation of the esophagus and esophageal hypersensitivity. Heartburn occurs in 25% of the American population monthly.
Endoscopy and esophageal pH monitoring are employed to assess heartburn. Certain causes of heartburn like Gastroesophageal reflux disease may be diagnosed based on symptoms alone. Possible differential diagnoses for heartburn are motility disorders ulcers esophagitis and medication side effects. Lifestyle modifications like weight reduction and avoiding fatty foods can help alleviate heartburn symptoms. For mild or intermittent heartburn over the counter alginates or antacids may be useful. Treatment of heartburn is mainly with antisecretory drugs such as H2-receptor antagonists and PPIs.
Basic effects of heartburn
A number of authors have documented cardiac failure in association with major burns and have emphasized the role of early myocyte damage during resuscitation. Myocyte destruction by inflammatory mediators and myocardial hypovolaemic ischemia have been proposed as etiologies for global cardiac dysfunction. It has not, to our knowledge, been evaluated in severe burns during the early resuscitation period of adequate fluid replacement whether regional cardiac dysfunction coexists with leakage of blood markers of myocyte damage, which is compulsory but not enough for the diagnosis of myocardial infarction and influences both treatment and outcome.
There are a number of challenges in diagnosis of acute myocardial disease in severe burns.
Accurate ECG tracings are usually impossible in a bandaged patient. Narcotics and sedatives, unconsciousness, thoracic and other injuries, and mechanical ventilation render it impossible both for the patient to report chest pain, and for the physician to make out the diagnosis of potential coexistent myocardial injury. The present application of troponin as a biomarker for the diagnosis of myocyte injury is clearly established in non-critically ill patients. It is unknown, however, whether the level is different in intensive care units due to confounding variables and also perhaps other underlying pathophysiological mechanisms.
Although raised troponin levels may signal myocardial damage, by themselves they are not an independent prognosticator of ICU or in-hospital death, and by themselves are unable to diagnose MI. In addition, diastolic dysfunction and myocardial stiffness in relation to thermal damage have been reported in animals and humans even without or prior to extensive systolic dysfunction but were not assessed with regional systolic function and potential marker leakage.
We hypothesized that also with adequate resuscitation in man, severe burn may accomplish localized regional myocardial dysfunction in addition to myocardial marker leakage, and may develop signs of diastolic dysfunction as evaluated by blood flow Doppler transoesophageal echocardiography. The aim of this study, therefore, was to examine the occurrence, timing, and incidence of regional wall motion abnormalities, flow indices of diastolic dysfunction, and troponin concentrations in patients with major burns during the early resuscitation period, using the Parkland formula.
Symptoms of pyrosis
Almax has been made in 169 patients suffering from heartburn. Clinical and endoscopic exploration revealed that 104 of the patients had an active duodenal ulcer and 60 of these were treated with antisecretory drugs plus Almax and 44 with Almax alone. Endoscopic exploration in the remaining 65 patients failed to reveal the presence of an ulcer and they were also treated with Almax alone. In all groups, Almax proved to be very effective and the majority of patients were symptom-free by the end of the two-week trial. 79.5% of the ulcer patients in group III required doses of 6-8 g/d whereas only 21.7% of those in group II with concomitant treatment with antisecretory drugs took more than 4 g/d.
The nonulcer patients of group I also used lower doses and only 29.3% needed to reach 6-8 g/d. There was a significant increase in daily bowel movements in all groups which was considered to be advantageous by most patients. Overall tolerance was excellent and side effects of diarrhea 7 cases, nauseous 5 cases and constipation 1 case were few and transient, and 84.2% of the patients expressed a clear preference for Almax over their previous antacid treatment.
Pyrosis is one of the typical symptoms of gastroesophageal reflux disease. In Spain, it has been reported that approximately one out of every three people has pyrosis regularly. Therefore, its diagnosis is of utmost importance. Pyrosis favorable response to empirical treatment with proton pump inhibitors allows for diagnosing it in the absence of alarm symptoms. If alarm signs are present, an upper gastrointestinal endoscope should be performed as soon as possible.
Treatment of heartburn
Lifestyle modifications like loss of weight and dietary changes to stop eating fatty heavy or spicy foods, especially at bedtime can alleviate symptoms. Antacids or alginates taken over-the-counter as needed can also alleviate mild or episodic heartburn. People might try to discontinue drugs that can exacerbate heartburn. Doctors can prescribe PPIs for 4-weeks to treat heartburn. H pylori if present can be eradicated. When one does not show a response to a PPI doctors use H2 receptor antagonists. As the person’s symptoms fade doctors may taper the dose or frequency of medicines.
Several medications have been used to heal heartburn but antisecretory drugs such as H2 receptor antagonists and PPIs have the greatest evidence for treating heartburn.
Antacids like those shown can be used to heal heartburn.
Antacids are quick-acting short-term treatments for heartburn consisting of preparations such as aluminum hydroxide magnesium hydroxide and calcium carbonate which neutralize acids. They were used generally in the past prior to the availability of more potent acid-reducing drugs for general, occasional post-meal heartburn or PRN. Alginate derived from seaweed and mixed with sodium or potassium bicarbonate is stronger than antacids for relief of heartburn.
As an adjunct in the treatment of GERD for the short term it has efficacy equal to PPIs. It is also used as an add-on treatment of partial PPI responders to enhance heartburn control and quality of life over PPIs alone. H2RAs suppress stomach acid by inhibiting histamine at certain receptors within the lining of the stomach. Their action lasts between 4 to 8 hours, depending on the drug. They are primarily utilized for rapid relief in individuals with mild acid reflux or as an added therapy in conjunction with PPIs, particularly at night as they are more effective at maintaining nighttime acid levels.
PPIs lower stomach acid by inhibiting an enzyme that participates in its creation and their action lasts considerably longer than H2RAs for about 16 to 18 hours. They are more potent and do not weaken with prolonged use. They don’t work right away and don’t correct the underlying cause of acid reflux they just render the refluxed material less acidic.
P-CABs are a more recent class of acid-reducing drugs that inhibit an enzyme used in acid production. Vonoprazan is the most studied P-CAB and is as effective as PPIs in healing esophagitis and preventing recurrence. In more severe conditions it might be even more effective than PPIs. P-CABs have not proved to be superior to a placebo in the treatment of symptoms among individuals with NERD, possibly because this condition encompasses a combination of various underlying conditions.