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20/11/2023

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17/01/2021

PEPTIC ULCER

Definition, Types and Pathology

💊Definition

👉An ulcer is defined as disruption of the mucosal integrity of the stomach and/or duodenum leading to a local defect or excavation due to active inflammation.
Ulcers are defined as a break in the mucosal surface >5 mm in size, with depth to the submucosa.

💊Types

PUD encompasses both

1⃣ gastric ulcers (GU)
2⃣ duodenal ulcers (DU)

💧Duodenal (DU) and gastric ulcers (GU) share many common features in terms of pathogenesis, diagnosis, and treatment, but several factors distinguish them from one another

💧Ulcers occur within the stomach and/or duodenum are often chronic in nature
(5 MARKS)
Pathology

💧Gastroduodenal Mucosal Defense
The gastric epithelium is under a constant assault by a series of endogenous noxious factors including hydrochloric acid (HCl), pepsinogen/pepsin, and bile salts.
In addition, a steady flow of exogenous substances such as medications, alcohol, and bacteria encounter the gastric mucosa.
💧A highly intricate biologic system is in place to provide defense from mucosal injury and to repair any injury that may occur.
💧The mucosal defense system is a three-level barrier, composed of pre epithelial, epithelial, and sub epithelial elements.
💧The first line of defense is a mucus-bicarbonate layer, which serves as a physicochemical barrier to multiple molecules including hydrogen ions.
💧Surface epithelial cells provide the next line of defense through several factors, including mucus production, epithelial cell ionic transporters that maintain intracellular pH and bicarbonate production, and intracellular tight junctions.
💧If the pre-epithelial barrier were breached, gastric epithelial cells bordering a site of injury can migrate to restore a damaged region (restitution).
💧Larger defects that are not effectively repaired by restitution require cell proliferation.
An elaborate microvascular system within the gastric submucosal layer is the key component of the subepithelial defense/repair system. A rich submucosal circulatory bed provides bicarbonate (HCO3⁺), which neutralizes the acid generated by parietal cell secretion of HCl.
Prostaglandins play a central role in gastric epithelial defense/repair. The gastric mucosa contains abundant levels of prostaglandins.
Hydrochloric acid and pepsinogen are the two principal gastric secretory products capable of inducing mucosal injury.

💊Epidemiology & Aetiology

✴Duodenal Ulcers (DU)

DUs are estimated to occur in 6 to 15% of the western population.
Before the discovery of H. pylori, the natural history of DUs was typified by frequent recurrences after initial therapy.
Eradication of H. pylori has greatly reduced these recurrence rates.
DUs occur most often in the first portion of duodenum (>95%), with ~90% located within 3 cm of the pylorus.
Malignant duodenal ulcers are extremely rare

✴Gastric Ulcers (GU)

GUs tends to occur later in life than duodenal lesions, with a peak incidence reported in the sixth decade.
More than half of GUs occurs in males.
Are less common than DUs, perhaps due to the higher likelihood of GUs being silent and presenting only after a complication develops.
Autopsy studies suggest a similar incidence of DUs and Gus.

💧In contrast to DUs, GUs can represent a malignancy.
Benign GUs associated with H. pylori are associated with antral gastritis.

💧In contrast, NSAID-related GUs are not accompanied by chronic active gastritis but may instead have evidence of a chemical gastropathy.

💊Aetiology

💧It is now clear that H. pylori and NSAID-induced injury account for the majority of DUs and Gus.
Gastric acid contributes to mucosal injury but does not play a primary role.

💧H. Pylori and Acid Peptic Disorders
Gastric infection with the bacterium H. pylori accounts for the majority of PUD.
This organism also plays a role in the development of gastric mucosal-associated lymphoid tissue (MALT) lymphoma and gastric adenocarcinoma.

💧It is still not clear how this organism, which is in the stomach, causes ulceration in the duodenum, or whether its eradication will lead to a decrease in gastric cancer.

💧NSAIDs-Induced Disease

NSAIDs represent one of the most commonly used medications

💧The spectrum of NSAID-induced morbidity ranges from nausea and dyspepsia to a serious gastrointestinal complication such as frank peptic ulceration complicated by bleeding or perforation.

💧Unfortunately, dyspeptic symptoms do not correlate with NSAID-induced pathology.
Over 80% of patients with serious NSAID-related complications do not have preceding dyspepsia.

💧In view of the lack of warning signs, it is important to identify patients who are at increased risk for morbidity and mortality related to NSAID usage.

✴Cigarette Smoking

Not only have smokers been found to have ulcers more frequently than do nonsmokers, but smoking appears to decrease healing rates, impair response to therapy and increase ulcer-related complications such as perforation.
The mechanism responsible for increased ulcer diathesis in smokers is unknown.

✴Genetic Predisposition

First-degree relatives of DU patients are three times as likely to develop an ulcer. However, the potential role of H. pylori infection in contacts is a major consideration.
Increased frequency in people with blood group O.

💧However, H. pylori preferentially bind to group O antibodies. Therefore, the role of genetic predisposition in common PUD has not been established

✴Psychological Stress
But studies examining the role of psychological factors in its pathogenesis have generated conflicting results.
Although PUD is associated with certain personality traits (neuroticism), these same traits are also present in individuals with non-ulcer dyspepsia (NUD) and other functional and organic disorders.
Although more work in this area is needed, no typical PUD personality has been found.

✴Diet
Certain foods can cause dyspepsia, but no convincing studies indicate an association between ulcer formation and a specific diet.
This is also true for beverages containing alcohol and caffeine

💧Conclusion

Multiple factors play a role in the pathogenesis of PUD

The two predominant causes are H. pylori infection and NSAID ingestion
Independent of the inciting or injurious agent, peptic ulcers develop as a result of an imbalance between mucosal protection/repair and aggressive factors
Gastric acid plays an essential role in mucosal injury

History
Epigastric pain – has poor predictive value for the presence of either DU or GU
Epigastric pain described as a burning or gnawing discomfort can be present in both DU and GU

The discomfort is also described as an ill-defined, aching sensation or as hunger pain.
The typical pain pattern in DU occurs 90 min to 3 hours after a meal and is frequently relieved by antacids or food

Pain that awakes the patient from sleep (between midnight and 3 A.M.) is the most discriminating symptom, with two-thirds of DU patients describing this complaint.
Unfortunately, this symptom is also present in one-third of patients with NUD.
The pain pattern in GU patients may be different from that in DU patients, where discomfort may actually be precipitated by food.

Nausea and weight loss occur more commonly in GU patients.

Dyspepsia that becomes constant, is no longer relieved by food or antacids, or radiates to the back may indicate a penetrating ulcer.
Sudden onset of severe, generalized abdominal pain may indicate perforation.
Pain worsening with meals, nausea, and vomiting of undigested food suggest gastric outlet obstruction.

Tarry stools or coffee ground emesis indicate bleeding.

💊Physical Examination

💧Epigastric tenderness is the most frequent finding in patients with GU or DU.

Physical examination is critically important for discovering evidence of ulcer complication. Tachycardia and orthostasis suggest dehydration secondary to vomiting or active gastrointestinal blood loss.

A severely tender, board like abdomen suggests perforation.

Presence of a succussion splash indicates retained fluid in the stomach, suggesting gastric outlet obstruction.

PUD-Related Complications
Gastrointestinal Bleeding is the most common complication.

Perforation is the second most common ulcer-related complication.

Pe*******on is a form of perforation in which the ulcer bed tunnels into an adjacent organ.
DUs tend to pe*****te posteriorly into the pancreas, leading to pancreatitis.

GUs tends to pe*****te into the left hepatic lobe.

Gastric Outlet Obstruction is the least common ulcer-related complication.
(10 MARKS)

💊Differential Diagnosis and Investigations

The most commonly encountered diagnosis among patients seen for upper abdominal discomfort is non-ulcer dyspepsia (NUD).
NUD, also known as functional dyspepsia or essential dyspepsia, refers to a group of heterogeneous disorders typified by upper abdominal pain without the presence of an ulcer.

Several additional disease processes that may present with ‘ulcer-like’ symptoms include

Gastroesophageal reflux

Pancreasticcobiliary disease (biliary colic, chronic pancreatitis)

Proximal gastrointestinal tumors

Vascular disease

Crohn's disease

💊Investigations

👉No investigation for peptic ulcer that can be done at the dispensary or health centre level, hence patients with suspected peptic ulcer should be referred for investigations.

👉Documentation of an ulcer requires either a
radiographic (barium study) or an endoscopic procedure.

👉Barium Meal

Barium studies of the proximal gastrointestinal tract are still commonly used as a first test for documenting an ulcer.

The sensitivity of older single-contrast barium meals for detecting a DU is as high as 80%, with a double-contrast study providing detection rates as high as 90%.
Radiographic studies that show a GU must be followed by endoscopy and biopsy.

👉Endoscopy (Esophagogastroduodenoscopy -OGD)

Provides the most sensitive and specific approach for examining the upper gastrointestinal tract.

Permits direct visualization of the mucosa, endoscopy facilitates photographic documentation of a mucosal defect and tissue biopsy to rule out malignancy (GU) or H. pylori

💊Diagnosis of H. Pylori

The tests for these are done in more specialized hospitals and may be for research purposes.

A number of H. pylori tests are available. They are classified as either non-endoscopy based or endoscopy based.

Non-endoscopy-based H. pylori tests are available.

H. pylori stool antigen test (HpSA)

Urea breathe test

Presence of antibodies to H. pylori in the serum

Three endoscopy-based H. pylori tests are available

Rapid urease test (RUT)

Bacterial culture H. pylori

Histologic detection of H. pylori in the biopsy specimen

💊DIFFERENTIAL DIAGNOSIS

👉GASTRITIS

👉ZOLLINGER ELLISONS DISEASE (CRCINOMA)

👉METASTASIS

👉METAPLASIA

👉Gastroesophageal reflux(STRICTURES)

👉Pancreasticcobiliary disease (biliary colic, chronic pancreatitis)(COMMON IN ALCOHOLICS SYMPTOMS ARE MOSTLY PATIEBNT IS JAUNDICED)

👉Proximal gastrointestinal tumors
Vascular disease(LIVER CIRHOSIS WHEREBY THERE PORTAL HYPERTENSION, WHICH MEANS THE BLOOD VESSELS AROUND THE ANTRUM OF THE GASTRIUM INCREASES ITS PRESSURE AND SUDDEN RUPTURES) PATIENT GET HEMETEMESIS - VOMITING BLOOD

👉Crohn's disease—GENETIC ULCERATIVE COLITIS WHEREBY THE SEROSA, MUCOSA BLEED INTERMITTENT)

💊Treatment

Essentially treatment is initiated at the hospital, at dispensary what is done is follow-up, and pre referral treatment of suspected PUD is the same as in Gastritis.

Before the discovery of H. pylori, the therapy of PUD disease was centered on the old dictum by Schwartz of ‘no acid, no ulcer.’

Although acid secretion is still important in the pathogenesis of PUD, eradication of H. pylori and therapy/prevention of NSAID-induced disease is the mainstay.

The clinician's goal in treating PUD is to

Provide relief of symptoms (pain or dyspepsia)

Promote ulcer healing

Prevent ulcer recurrence and complications
Once an ulcer (GU or DU) is documented, then the main issue at stake is whether H. pylori or an NSAID is involved.
With H. pylori present, independent of the NSAID status, triple therapy is recommended for 14 days, followed by continued acid-suppressing drugs (H2 receptor antagonist or PPIs) for a total of 4 to 6 weeks.

💧Therapy for H. Pylori

H. pylori should be eradicated in patients with documented PUD

This holds true independent of time of presentation (first episode or not), severity of symptoms, presence of confounding factors such as ingestion of NSAIDs, or whether the ulcer is in remission.

Documented eradication of H. pylori in patients with PUD is associated with a dramatic decrease in ulcer recurrence.

Combination therapy for 14 days provides the greatest efficacy.

The agents used with the greatest frequency include amoxicillin, metronidazole, tetracycline, clarithromycin, and bismuth compounds.

💊Triple Therapy

The most common regime in our environment is Amoxillin, Metronidazole and omeprazole other regimens include

✴Lansoprazole, clarithromycin, and amoxicillin

✴Bismuth subsalicylate, tetracycline, and metronidazole etc.

Dosing
1⃣. Amoxillin 500 mg PO every 8 hours
2⃣.Metronidazole 400 mg PO every 8 hours
3⃣.Clarithromycin 500 mg PO every 12 hours
4⃣.Omeprazole 20 mg once a day
5⃣Lansoprazole 20-40 mg once a day

💧Therapy of NSAID-Related Gastric or Duodenal Injury

Medical intervention for NSAID-related mucosal injury includes treatment of an active ulcer and prevention of future injury.

Ideally the injurious agent should be stopped as the first step in the therapy of an active NSAID-induced ulcer.

If that is possible, then treatment with one of the acid inhibitory agents (H2 blockers or PPIs) is indicated.

Cessation of NSAIDs is not always possible because of the patient's severe underlying disease (e.g. Arthritis).

Only PPIs can heal GUs or DUs, independent of whether NSAIDs are discontinued.

Prevention of NSAID-induced ulceration can be accomplished by misoprostol (200µg qid) or a PPI.

High-dose H2 blockers (famotidine, 40 mg bid) have also shown some promise.

Response to Therapy
The majority (>90%) of GUs and DUs heal with the conventional therapy outlined above
GU that fails to heal after 12 weeks and a DU that doesn't heal after 8 weeks of therapy should be considered refractory.

Once poor compliance and persistent H. pylori infection have been excluded, NSAID use, either inadvertent or surreptitious, must be excluded.

In addition, cigarette smoking must be eliminated.
For a GU, malignancy must be meticulously excluded.
More than 90% of refractory ulcers (either DUs or GUs) heal after 8 weeks of treatment with higher doses of PPI (omeprazole, 40 mg/d). This higher dose is also effective in maintaining remissio.

Anti Ulcer Drugs and Surgical Treatment of PUD

Details on Individual Drug Classes

Acid Neutralizing/Inhibitory Drugs-Antacids
They are now rarely, if ever, used as the primary therapeutic agent but instead are often used by patients for symptomatic relief of dyspepsia.
The most commonly used agents are mixtures of aluminum hydroxide and magnesium hydroxide.

Aluminum hydroxide can produce constipation and phosphate depletion; magnesium hydroxide may cause loose stools.
Many of the commonly used antacids have a combination of both aluminum and magnesium hydroxide in order to avoid these
side effects.

H2 Receptor Antagonists
Four of these agents are presently available (cimetidine, ranitidine, famotidine, and nizatidine). Although each has different potency, all will significantly inhibit basal and stimulated acid secretion to comparable levels when used at therapeutic doses.
Moreover, similar ulcer-healing rates are achieved with each drug when used at the correct dosage.

✴This class of drug is often used for treatment of active ulcers (4 to 6 weeks) in combination with antibiotics directed at eradicating H. pylori.
Dosing

Cimetidine 300 mg four times per day
Ranitidine, famotidine, and nizatidine are more potent H2 receptor antagonists than cimetidine
Each can be used once a day at bedtime

Comparable nighttime dosing regimens are ranitidine, 300 mg, famotidine, 40 mg, and nizatidine, 300 mg

👉Proton Pump Inhibitors (PPIs)

Omeprazole, lansoprazole, rabeprazole and lansoprazole.

These are the most potent acid inhibitory agents available.

Because the pumps need to be activated for these agents to be effective, their efficacy is maximized if they are administered before a meal (e.g. in the morning before breakfast).
Standard dosing for omeprazole and lansoprazole is 20 mg and 30 mg once per day respectively.

Cytoprotective Agents

Sucralfate

This compound is insoluble in water and becomes a viscous paste within the stomach and duodenum, binding primarily to sites of active ulceration.

It should be avoided in patients with chronic renal insufficiency to prevent aluminum-induced neurotoxicity.
Standard dosing of Sucralfate is 1 g four times per day.

Bismuth-Containing Preparations
The resurgence in the use of these agents is due to their effect against H. pylori.
Colloidal bismuth sub citrate (CBS) and bismuth subsalicylate (BSS) are the most widely used preparations.

✴The mechanism by which these agents induce ulcer healing is unclear.

Potential mechanisms include ulcer coating; prevention of further pepsin/HCl-induced damage; binding of pepsin; and stimulation of prostaglandins, bicarbonate, and mucous secretion.

Long-term usage with high doses, especially with the avidly absorbed CBS, may lead to neurotoxicity.

These compounds are commonly used as one of the agents in an anti-H. pylori regimen.

Prostaglandin Analogues

In view of their central role in maintaining mucosal integrity and repair, stable prostaglandin analogues were developed for the treatment of PUD.

The prostaglandin E1 derivative misoprostol is used in the prevention of NSAID-induced gastroduodenal mucosal injury.

The mechanism by which this rapidly absorbed drug provides its therapeutic effect is through enhancement of mucosal defense and repair.
Misoprostal is contraindicated in women who may be pregnant.

The standard therapeutic dose is 200 µg four times per day.

💊Surgical Therapy

Surgical intervention in PUD can be viewed as being either

Elective, for treatment of medically refractory disease

Urgent/emergent, for the treatment of an ulcer-related complication
Refractory ulcers are an exceedingly rare occurrence

Surgery is more often required for treatment of an ulcer-related complication

✴Gastrointestinal bleeding, perforation, and gastric outlet obstruction are the three complications that may require surgical intervention

By Vanessa!

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27/08/2020

LUNG ABSCESS ( new notes )

LUNG ABSCESS
Definition
👉Lung abscess is defined as necrosis of the pulmonary tissue and formation of cavities containing necrotic debris or fluid caused by microbial infection.

👉The formation of multiple small (A preexisting condition (e.g. obstruction)
>Spread from an extrapulmonary site
>Bronchiectasis
>An immunocompromised state
👉Lung abscesses can be further characterized by the responsible pathogen, such as:
> Staphylococcus lung abscess
>Anaerobic infections
>Aspergillus lung abscess

✳Pathophysiology

👉Most frequently, the lung abscess arises as a complication of aspiration pneumonia caused by mouth anaerobes.

👉A bacterial inoculum from the gingival crevice reaches the lower airways, and infection is initiated because the bacteria are not cleared by the patient's host defense mechanism.

👉This results in aspiration pneumonitis and progression to tissue necrosis 7-14 days later, resulting in formation of lung abscess

👉Other mechanisms for lung abscess formation include bacteremia or tricuspid valve endocarditis, causing septic(CONSISTS OF BACTERIA MOSTLY β HEMOLYTIC STREPTOCOCCI VIRIDANS) emboli (usually multiple) to the lung.

👉The oral anaerobe fusobacterium necrophorum is the most common pathogen.

✳Risks of Developing Lung Abscess

👉Patients at the highest risk for developing lung abscess have the following risk factors:
>Periodontal disease
>Seizure disorder
>Alcohol abuse
>Dysphagia
>Other patients at high risk for developing lung abscess include individuals with an inability to protect their airways from massive aspiration because of a diminished gag or cough reflex, caused by a state of impaired consciousness (e.g. from alcohol or other CNS depressants, general anesthesia, or encephalopathy)

✳Causes of Lung Abscess
👉An abscess may develop as an infectious complication of a preexisting bulla or lung cyst.

👉An abscess may develop secondary to carcinoma of the bronchus; the bronchial obstruction causes post obstructive pneumonia, which may lead to abscess formation.

👉Published reports since the beginning of the antibiotic area have established that anaerobic bacteria are the most significant pathogens in lung abscess. The most common anaerobes are

>Peptostreptococcus species
>Bacteroides species
>Fusobacterium species
>Microaerophilic streptococci

👉Aerobic bacteria that may infrequently cause lung abscess include

>Staphylococcus aureus
>Streptococcus pyogenes
>Streptococcus pneumoniae (rarely)
>Klebsiella pneumoniae
>Haemophilus influenzae
>Pseudomonas aeruginosa
>Actinomyces species
>Nocardia species
>Gram-negative bacilli
👉Nonbacterial and atypical bacterial pathogens may also cause lung abscesses, usually in the immunocompromised host these microorganisms include
>Parasites (Paragonimus and Entamoeba species)
>Fungi (e.g. Aspergillus, Cryptococcus, Histoplasma, Blastomyces, and Coccidioides species) COMMON OPPORTUNISTIC INFECTIONS IN HIV AID 3-4 STAGE
>Mycobacterium species

✳Epidemiology of Lung Abscess

👉Frequency

The frequency of lung abscess in the general population is not known.
👉Sex

A male predominance for lung abscess is reported in published case series.
👉Age

Lung abscesses likely occur more commonly in elderly patients because of the increased incidence of periodontal disease and the increased prevalence of dysphagia and aspiration.

✳Mortality/Morbidity

👉Most patients with primary lung abscess improve with antibiotics, with cure rates documented at 90-95%

👉Host factors associated with a poor prognosis include advanced age, debilitation, malnutrition, human immunodeficiency virus infection or other forms of immunosuppression, malignancy, and duration of symptoms greater than 8 weeks.

👉The mortality rate for patients with underlying immunocompromised status or bronchial obstruction who develop lung abscess may be as high as 75%.

👉Frequently hospital acquired aerobic organisms are associated with poor outcomes

✳Clinical Features of Lung Abscess

⏹History

Symptoms depend on whether the abscess is caused by anaerobic or other bacterial infection.

👉Anaerobic infection in lung abscess

>Patients often present with indolent symptoms that evolve over a period of weeks to months.
>The usual symptoms are fever, cough with purulent and copious sputum production, night sweats, anorexia, and weight loss.
>The expectorated sputum characteristically is foul smelling and bad tasting.
>Patients may develop hemoptysis or pleurisy.

👉Other pathogens in lung abscess

>These patients generally present with conditions that are more emergent in nature and are usually treated while they have bacterial pneumonia.
>Cavitation occurs subsequently as parenchymal necrosis ensues.
>Abscesses from fungi, Nocardia species, and Mycobacteria species tend to have an indolent course and gradually progressive symptoms.

✳Physical Examination

👉The findings on physical examination of a patient with lung abscess are variable.

👉Physical findings may be secondary to associated conditions such as underlying pneumonia or pleural effusion.

👉Patients with lung abscesses may have low-grade fever in anaerobic infections and temperatures higher than 38.5°C in other infections.

👉Generally, patients with in lung abscess have evidence of gingival disease.

👉Clinical findings of concomitant consolidation may be present (e.g. dullness to percussion, bronchial breath sounds, course inspiratory crackles)

👉Evidence of pleural friction rub and signs of associated pleural effusion, empyema, and pyopneumothorax may be present. Signs include contra-lateral shift of the mediastinum, dullness to percussion, and absent breath sounds over the effusion.

👉Digital clubbing may develop rapidly

✳Diagnosis and Management of Lung Abscess

➖Differential Diagnosis

👉Pulmonary tuberculosis
👉Empyema thoracis
👉Lung cancer
👉Pneumonia
👉Pulmonary embolism
👉Infective Endocarditis
👉Pneumocystis Jirovecii Pneumonia (Pneumocystis Carinii Pneumonia)
👉Wegener Granulomatosis
👉Hydatid Cysts (ECHINOCCCUS GRANULOSIS, ECHINOCOCCUS MULTICULARIS GROUP OF TAPE WORMS0

✳Diagnosis of Lung Abscess

Refer the patient to higher centre for laboratory studies and imaging studies

👉CBC (FULL BLOOD PICTURE,
👉Chest X-RAY,
👉SPUTUM FOR CULTURE AND SENSITIVITY)


✳💊Treatment

⏺Perform pre - referral treatment

👉IV fluids

👉Antibiotics (START WITH PENICILLINC 5 MU IV 6HOURLY FOR AT LEAST 4 DAYS , THEN ORAL GIVE TAB AUGUMENTIN (CLAVULENIC + AMOXYCILLIN) THIS MEDICATION IS GOOD FOR BACTERIAS WHICH PRODUCE β LACTAMASE ANTAGONISM. and

👉 Analgesics

👉Monitor vital signs
ALSO ADD TAB METRONIDAZOLE (FLAGYL) 400MG ORALLY TDS 7 DAYS
🔼Refer the patient to higher centre (hospital) for proper management

✳Prevention

👉Prevention of aspiration is important to minimize the risk of lung abscess.

👉Early intubation in patients who have diminished ability to protect the airway from massive aspiration (cough, gag reflexes), should be considered.

👉Positioning patient in the supine position at a 30° reclined angle minimizes the risk of aspiration. Vomiting patients should be placed on their sides.

👉Improving oral hygiene and dental care in elderly and debilitated patients may decrease the risk of anaerobic lung abscess.

✳💥Complications of Pulmonary Abscess

👉Rupture into pleural space causing
👉empyema
👉Pleural fibrosis
👉Trapped lung
👉Respiratory failure
👉Bronchopleural fistula
👉Pleural cutaneous fistula
👉In a patient with coexisting empyema and lung abscess, draining the empyema while continuing prolonged antibiotic therapy is often necessary

✳💥Prognosis

👉The prognosis for lung abscess following antibiotic treatment is generally favorable.
Over 90% of lung abscesses are cured with medical management alone, unless caused by bronchial obstruction secondary to carcinoma.

By Dr Vanessa
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26/08/2020

DIABETIC KETOACIDOSIS (DKA)

⏩Diabetic ketoacidosis is an acute metabolic complication of diabetes characterized by hyperglycemia, hyperketonemia, and metabolic acidosis. Hyperglycemia causes an osmotic diuresis with significant fluid and electrolyte loss. DKA occurs mostly in type 1 diabetes mellitus (DM). It causes nausea, vomiting, and abdominal pain and can progress to cerebral edema, coma, and death. DKA is diagnosed by detection of hyperketonemia and anion gap metabolic acidosis in the presence of hyperglycemia. Treatment involves volume expansion, insulin replacement, and prevention of hypokalemia.

⏺(See also Diabetes Mellitus and Complications of Diabetes Mellitus.)

Diabetic ketoacidosis (DKA) is most common among patients with type 1 diabetes mellitus and develops when insulin levels are insufficient to meet the body’s basic metabolic requirements. DKA is the first manifestation of type 1 DM in a minority of patients. Insulin deficiency can be absolute (eg, during lapses in the administration of exogenous insulin) or relative (eg, when usual insulin doses do not meet metabolic needs during physiologic stress).

⏺Common physiologic stresses that can trigger DKA include

⏩Acute infection (particularly pneumonia and U.T.I)
⏩Myocardial infarction
⏩Stroke
⏩Pancreatitis
⏩Trauma

⏺Some drugs implicated in causing DKA include

⏩Corticosteroids
⏩Thiazide diuretics
⏩Sympathomimetics
⏩Sodium-glucose co-transporter 2 (SGLT-2) inhibitors

DKA is less common in type 2 diabetes mellitus, but it may occur in situations of unusual physiologic stress. Ketosis-prone type 2 diabetes is a variant of type 2 diabetes, which is sometimes seen in obese patients, often of African (including African-American or Afro-Caribbean) origin. People with ketosis-prone diabetes (also referred to as Flatbush diabetes) can have significant impairment of beta cell function with hyperglycemia, and are therefore more likely to develop DKA in the setting of significant hyperglycemia. SGLT-2 inhibitors have been implicated in causing DKA in both type 1 and type 2 DM.

PATHOPHYSIOLOGY

✳Insulin deficiency causes the body to metabolize triglycerides and amino acids instead of glucose for energy. Serum levels of glycerol and free fatty acids rise because of unrestrained lipolysis, as does alanine because of muscle catabolism. Glycerol and alanine provide substrate for hepatic gluconeogenesis, which is stimulated by the excess of glucagon that accompanies insulin deficiency.

✳Glucagon also stimulates mitochondrial conversion of free fatty acids into ketones. Insulin normally blocks ketogenesis by inhibiting the transport of free fatty acid derivatives into the mitochondrial matrix, but ketogenesis proceeds in the absence of insulin. The major ketoacids produced, acetoacetic acid and beta-hydroxybutyric acid, are strong organic acids that create metabolic acidosis. Acetone derived from the metabolism of acetoacetic acid accumulates in serum and is slowly disposed of by respiration.

✳Hyperglycemia due to insulin deficiency causes an osmotic diuresis that leads to marked urinary losses of water and electrolytes. Urinary excretion of ketones obligates additional losses of sodium and potassium. Serum sodium may fall due to natriuresis or rise due to excretion of large volumes of free water. Potassium is also lost in large quantities, sometimes > 300 mEq/24 h (300 mmol/24 h). Despite a significant total body deficit of potassium, initial serum potassium is typically normal or elevated because of the extracellular migration of potassium in response to acidosis. Potassium levels generally fall further during treatment as insulin therapy drives potassium into cells. If serum potassium is not monitored and replaced as needed, life-threatening hypokalemia may develop.

SYMPTOMS and SIGNS

Symptoms and signs of diabetic ketoacidosis include symptoms of hyperglycemia with the addition of nausea, vomiting, and—particularly in children—abdominal pain. Lethargy and somnolence are symptoms of more severe decompensation. Patients may be hypotensive and tachycardic due to dehydration and acidosis; they may breathe rapidly and deeply to compensate for acidemia (Kussmaul respirations). They may also have fruity breath due to exhaled acetone. Fever is not a sign of DKA itself and, if present, signifies underlying infection. In the absence of timely treatment, DKA progresses to coma and death.

Acute cerebral edema, a complication in about 1% of DKA patients, occurs primarily in children and less often in adolescents and young adults. Headache and fluctuating level of consciousness herald this complication in some patients, but respiratory arrest is the initial manifestation in others. The cause is not well understood but may be related to too-rapid reductions in serum osmolality or to brain ischemia. It is most likely to occur in children < 5 yr when DKA is the initial manifestation of diabetes mellitus. Children with the highest BUN and lowest Paco2 at presentation appear to be at greatest risk. Delays in correction of hyponatremia and the use of bicarbonate during DKA treatment are additional risk factors.

DIAGNOSIS

✳Arterial pH
✳Serum ketones
✳Calculation of anion gap

In patients suspected of having diabetic ketoacidosis, serum electrolytes, BUN and creatinine, glucose, ketones, and osmolarity should be measured. Urine should be tested for ketones. Patients who appear significantly ill and those with positive ketones should have arterial blood gas measurement.

DKA is diagnosed by an arterial pH < 7.30 with an anion gap > 12 (see Acid-Base Disorders : Calculation of the anion gap) and serum ketones in the presence of hyperglycemia. A presumptive diagnosis can be made when urine glucose and ketones are strongly positive. Urine test strips and some assays for serum ketones may underestimate the degree of ketosis because they detect acetoacetic acid and not beta-hydroxybutyric acid, which is usually the predominant ketoacid.

Symptoms and signs of a triggering illness should be pursued with appropriate studies (eg, cultures, imaging studies). Adults should have an ECG to screen for acute myocardial infarction and to help determine the significance of abnormalities in serum potassium.

Other laboratory abnormalities include hyponatremia, elevated serum creatinine, and elevated plasma osmolality. Hyperglycemia may cause dilutional hyponatremia, so measured serum sodium is corrected by adding 1.6 mEq/L (1.6 mmol/L) for each 100 mg/dL (5.6 mmol/L) elevation of serum glucose over 100 mg/dL (5.6 mmol/L). To illustrate, for a patient with serum sodium of 124 mEq/L (124 mmol/L) and glucose of 600 mg/dL (33.3 mmol/L), add 1.6 ([600 −100]/100) = 8 mEq/L (8 mmol/L) to 124 for a corrected serum sodium of 132 mEq/L (132 mmol/L). As acidosis is corrected, serum potassium drops. An initial potassium level 7.3.

👉Hypokalemia prevention
Hypokalemia prevention requires replacement of 20 to 30 mEq potassium in each liter of IV fluid to keep serum potassium between 4 and 5 mEq/L (4 and 5 mmol/L). If serum potassium is < 3.3 mEq/L (3.3 mmol/L), insulin should be withheld and potassium given at 40 mEq/h until serum potassium is ≥ 3.3 mEq/L (3.3 mmol/L); if serum potassium is > 5 mEq/L (5 mmol/L), potassium supplementation can be withheld.

Initially normal or elevated serum potassium measurements may reflect shifts from intracellular stores in response to acidemia and belie the true potassium deficits that almost all patients with diabetic ketoacidosis have. Insulin replacement rapidly shifts potassium into cells, so levels should be checked hourly or every other hour in the initial stages of treatment.

Other measures

👉Hypophosphatemia often develops during treatment of DKA, but phosphate repletion is of unclear benefit in most cases. If indicated (eg, if rhabdomyolysis, hemolysis, or neurologic deterioration occurs), potassium phosphate, 1 to 2 mmol/kg of phosphate, can be infused over 6 to 12 h. If potassium phosphate is given, the serum calcium level usually decreases and should be monitored.

👉Treatment of suspected cerebral edema is hyperventilation, corticosteroids, and mannitol, but these measures are often ineffective after the onset of respiratory arrest.

Treatment reference
1. Kitabchi AE, Umpierrez GE, Miles JM, et al: Hyperglycemic crises in adult patients with diabetes. Diabetes Care 32: 1335–1343, 2009.

KEY POINTS

👉Acute physiologic stressors (eg, infections, myocardial infarction) can trigger acidosis, moderate glucose elevation, dehydration, and severe potassium loss in patients with type 1 diabetes.

👉Acute cerebral edema is a rare (about 1%) but lethal complication, primarily in children and less often in adolescents and young adults.

👉Diagnose by an arterial pH < 7.30, with an anion gap > 12 and serum ketones in the presence of hyperglycemia.

👉Acidosis typically corrects with IV fluid and insulin; consider bicarbonate only if marked acidosis (pH < 7) persists after 1 h of therapy.
Withhold insulin until serum potassium is ≥ 3.3 mEq/L (3.3 mmol/L).


By Dr. Vanessa
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