GASTROENTEROLOGICAL SURGICAL EMERGENCIES

Peptic ulcer disease and gastrointestinal bleeding

While overall hospitalizations related to peptic ulcer disease have declined over the past 3 decades, this entity remains a common cause of intensive care unit (ICU) admission in the United States.1 The symptomatic manifestations of gastroduodenal ulcers can broadly be divided into 2 categories-bleeding and perforation. Bleeding, as a result of ulcer erosion into vascular structures, for which patients will require ICU admission for airway protection and resuscitation in the setting of hemorrhagic shock. Perforation, as a result of full-thickness ulceration, which will invariably cause intra-abdominal sepsis and require operative intervention with subsequent ICU admission for the management of distributive shock.2

Severe hemorrhage as a result of peptic ulcer disease will typically manifest clinically with some combination of epigastric pain, tachycardia, hypotension, and anemia, as well as hematemesis or blood per rectum. Management is focused on hemodynamic stabilization, correction of the underlying coagulopathy, and airway protection with endotracheal intubation in patients at risk for aspiration as a result of hematemesis.3 The most important intervention with respect to decreasing patient mortality is performance of upper endoscopy, which will localize and treat the underlying source of hemorrhage.4 Recurrent bleeding is a common problem among patients with bleeding ulcers and requires vigilance at bedside for signs and symptoms of ongoing gastrointestinal bleeding (GIB). Repeat endoscopy and angioembolization in the interventional radiology suite are management options for the bleeding ulcer that remains treatment resistant to an initial trial of endoscopic management. Surgical intervention for management of the bleeding ulcer is exceedingly uncommon in the current era of facile endoscopic intervention. While laparoscopic approaches have been described for management of bleeding ulcers, the most common surgical approach remains laparotomy with subsequent ligation of bleeding vessels for duodenal ulcers or resection of diseased tissue for gastric ulcers.5 Postoperatively, patients will classically have an early period of resuscitation and then a fast recovery with transition out of the ICU. Nutrition may be a challenge in these patients as they may require a prolonged period of nil per os (NPO) and may require distal feeding access with jejunostomy or, less ideally, total parenteral nutrition.

Perforated peptic ulcers typically present with acute-onset abdominal pain with peritonitis, fever, tachycardia, hypotension, leukocytosis, and pneumoperitoneum on diagnostic imaging. Excluding the rare case of a "contained" perforation of a gastroduodenal ulcer on imaging, the vast majority of patients require emergent surgical intervention for repair of the perforation and source control of intra-abdominal sepsis. In contrast to patients with bleeding ulcers, perforated ulcers can commonly be managed in a minimally invasive fashion with laparoscopic surgery. Postoperatively, patients may not require ICU admission unless they have ongoing septic shock as a result of intra-abdominal contamination. Patients will require pharmacologic acid suppression with a proton pump inhibitor (PPI) or histamine H₂-receptor antagonists, and antimicrobial therapy covering gram-negative aerobic and anaerobic bacteria. The role of antifungal therapy in the management of perforated peptic ulcers remains a matter of debate.6 Surgical nutrition is an even greater challenge in these patients, as they will almost certainly be NPO until it can be demonstrated that the perforation is resolved and malnutrition is independently associated with adverse patient outcomes.7 Classically, patients will undergo an orally contrasted study on postoperative days 3 to 5 before trialing oral nutrition, increasing the risk of postoperative malnutrition and the increased risks of associated complications.8 The astute surgeon will create a plan for distal feeding access, again with jejunostomy or gastrojejunostomy, at the time of the index operation. Patients will commonly maintain a nasogastric tube for decompression until confirmation that a gastroduodenal perforation is healed.

A special consideration with respect to GIB in the ICU setting is stress or erosive gastritis, which is an extremely common condition in critically ill patients. Decreased splanchnic perfusion as a result of hypotension or use of vasopressor agents is common in critically ill patients and causes erosion of the gastric mucosa and submucosa. These lesions, known as stress ulcers, are extremely common among critically ill patients and have been demonstrated via endoscopy to be present in the vast majority of ICU patients. However, less than 5% of patients with these lesions develop clinically significant GIB.9 Given that few ICU patients with stress ulcers go on to develop symptoms from these lesions, management primarily focuses on preventing symptoms in high-risk patients, such as patients with prolonged courses of mechanical ventilation, coagulopathy, or significant burn injury.

Esophageal varices

Bleeding esophageal varices are the most lethal complication of portal venous hypertension among patients with cirrhosis of the liver and are associated with an extremely high mortality.10 Esophageal varices are the consequence of the development of extensive high pressure portosystemic collaterals between the coronary vein and the azygos vein and are present in approximately 85% of patients with decompensated cirrhosis.11 This high pressure collateral system allows for the development of venous varicosities within the distal esophagus that are prone to erosion and rupture, resulting in massive hematemesis and GIB that culminate in shock and exsanguination.

Management of esophageal variceal bleeding is focused on balanced resuscitation with blood products, reversal of underlying coagulopathy, endoscopic banding to control bleeding, and medical therapy to promote splanchnic vasoconstriction and prevent bacterial peritonitis among patients who survive initial hemorrhage.12 Among patients who continue to have upper GIB despite banding as well as other symptoms of portal hypotension, transjugular intrahepatic portosystemic shunt (TIPS) is an endovascular intervention that reduces portal hypertension by providing a new route of portal venous drainage into the systemic circulation.13

Intestinal ischemia

Mesenteric ischemia is a common disease of critically ill patients with exceedingly high morbidity and mortality.14 While the causes of mesenteric ischemia can be subdivided into arterial thromboembolic, venous thrombotic, and nonocclusive disease, the final common pathway of all etiologies is hypoperfusion of the small bowel leading to ischemia, inflammation, and the potential for necrosis and perforation.

Among patients presenting to the emergency department, arterial thromboembolism is the most common cause of mesenteric ischemia.15 In these patients, embolism from the left atrium (in the setting of atrial fibrillation) or rupture of atherosclerotic plaque within the superior mesenteric artery (SMA) leads to occlusion of the SMA with subsequent ischemia of the jejunum, ileum, and right colon.

In contrast, among critically ill patients, the most common cause of mesenteric ischemia is nonocclusive mesenteric ischemia (NOMI). Classically, a disease of the patient in vasopressor-dependent shock, NOMI patients experience arteriolar vasoconstriction as blood is shunted away from the splanchnic vascular bed to facilitate coronary and central nervous system perfusion.

Venous thrombosis is an uncommon cause of mesenteric ischemia, classically found among patients with inherited or acquired hypercoagulability disorders. These patients form de novo thrombus within the portal or superior mesenteric veins (SMVs), leading to venous stasis and subsequent intestinal ischemia as a result of outflow obstruction.16

With some exceptions, the clinical presentation is similar among patients with all 3 etiologies of mesenteric ischemia. Patients present with "pain out of proportion to physical examination," a frustrating misnomer meant as severe abdominal discomfort without tenderness to palpation but often interpreted by clinicians to mean severe tenderness. Mesenteric ischemia elicits severe visceral pain without concomitant peritoneal inflammation, which explains the absence of peritonitis in cases excluding those which have advanced to intestinal necrosis and perforation. Additional findings include tachycardia, hypotension, leukocytosis, differential with neutrophil predominance and bandemia, acute kidney injury, and a defined vascular lesion on computed tomography (CT) angiography of the abdomen and pelvis.

Management pathways markedly differ on the basis of the particular etiology of mesenteric ischemia, but the core principles remain restoration of splanchnic perfusion and resection of nonviable ischemic intestine.

Arterial thromboembolism is classically managed with laparotomy and open revascularization of the SMA, either with embolectomy or bypass. Advances in endovascular management have increased the variety of available treatment options to include percutaneous thrombectomy with or without stenting as well as the same procedure via an open retrograde approach for patients with lesions at the origin of the SMA.17 Venous occlusion in the setting of portal venous thrombus or SMV thrombus is typically managed with therapeutic anticoagulation, most commonly unfractionated heparin. A small subset of patients are candidates for catheter-directed thrombolysis with a continuous infusion of tissue plasminogen activator (tPA), though patient selection for this intervention remains a subject of debate.18

NOMI is perhaps the most challenging of these pathologies to manage in that there is no defined lesion to treat surgically; rather, ischemia is the result of profound critical illness leading to a low-flow state in the splanchnic vascular bed and mismatch between oxygen delivery and demand. Targeted therapies have been described for reversal of arteriolar vasoconstriction, most commonly catheter-directed infusion of vasodilating agents to prevent and reverse vasospasm. However, there is scant literature demonstrating mortality benefit to patients undergoing this treatment.19 The essence of NOMI management remains expedient reversal of the underlying cause of critical illness and shock.

Intestinal obstruction

Bowel obstruction is a common cause of hospitalization and among the most common indications for surgery in the United States but is a rare cause of ICU admission.20 Mechanical obstruction of the small bowel is typically caused by extrinsic compression. In the United States, the most common cause is intra-abdominal adhesions from prior surgery while worldwide the most common etiology of small bowel obstruction is incarcerated hernia. Bowel obstruction prevents the anterograde progression of enteric contents, leading to small bowel dilatation. This dilatation of the bowel proximal to the transition point of obstruction results in the classic colicky abdominal pain, as well as nausea and bilious emesis. Increasing dilatation of the intestine results in mesenteric venous stasis and intestinal ischemia, ultimately resulting in intestinal ischemia with peritonitis and perforation if the obstruction fails to resolve.

Patients who present with peritonitis or patients with clinical and laboratory evidence of intestinal ischemia, as well as patients who present with obstructions as a result of hernia or closed loop obstructions, should be taken to the operating room for operative intervention. Patients who present with more benign symptoms not concerning for intestinal ischemia can potentially be managed nonoperatively with nasogastric decompression, fluid resuscitation, and serial abdominal examinations. The majority of patients managed nonoperatively undergo resolution of their bowel obstruction with nasogastric decompression. Recent literature has supported the use of oral contrast challenge to identify patients in whom a trial of nonoperative management will not be successful.21 In the described oral contrast challenge, a patient identified as a candidate for nonoperative management will undergo a 4-hour period of nasogastric decompression and then be administered an oral bolus of water-soluble contrast. The passage of this contrast is then monitored with intermittent abdominal x-ray study. Patients who fail to pass contrast to the cecum after 48 hours of nonoperative management are unlikely to resolve their bowel obstruction with continued observation and will likely need operative intervention for resolution of their obstruction.

Operative intervention for small bowel obstruction can be performed with laparoscopy or with an open approach via laparotomy. Laparoscopic intervention is a reasonable approach for patients with adhesive small bowel obstructions and a relatively nondilated bowel pattern but can be challenging for patients with diffusely dilated bowel, which can preclude establishment of a laparoscopic working space. Division of adhesive bands will resolve obstruction. Intestine with ischemia or necrosis will necessitate resection and anastomosis. Postoperatively, patients will typically continue nasogastric decompression until they have return of bowel function and then will be advanced on their diet as tolerated.

Obstructions of the large intestine require brief special consideration. The anatomic border between the small intestine and the colon is the ileocecal valve, a one-way valve that permits the transit of small bowel contents into the colon but precludes retrograde flow of colonic stool into the small bowel. Unlike small bowel obstructions, which are most commonly managed nonoperatively via nasogastric decompression, the large intestine cannot be effectively decompressed with a nasogastric tube when an obstruction is preventing anterograde flow of colonic contents, as the ileocecal valve will prevent retrograde decompression. Because the colon cannot be decompressed via noninvasive means, colonic obstruction will progressively worsen until colonic perforation occurs as a result of increasing bowel wall tension, a pathology that classically occurs at the thin-walled cecum. Operative management of large bowel obstructions typically involves resection of the obstructing pathology when it is feasible (eg, diverticular stricture) or proximal diversion with colostomy in cases where it is not (eg, a newly diagnosed colonic malignancy with metastatic disease).21

Biliary emergencies

Benign biliary disease is a highly prevalent pathology in the United States that most commonly manifests as biliary colic, a disease managed with routine outpatient cholecystectomy. Benign biliary disease progresses to profound critical illness when patients develop biliary obstruction with infection (obstructive cholangitis) or with septic shock as a result of severe gallbladder infection (gangrenous cholecystitis).

The development of cholangitis requires biliary obstruction and bacterial infection of nondraining bile within the obstructed biliary tree.22 This pathology typically results in severe systemic infection and clinically manifests as Reynold's pentad of fever, right upper-quadrant pain, jaundice, altered mental status, and distributive shock. The core of the management of this disease is prompt resuscitation and antibiotics targeted at gram-negative and anaerobic bacteria. Following initial stabilization, patients should undergo prompt biliary decompression. While surgical means of decompression have been described (eg, open common bile duct exploration), contemporary management of this disease revolves around either endoscopic decompression with endoscopic retrograde cholangiopancreatography (ERCP) or in situations where that is not possible (eg, in the case of a nontraversable malignant biliary obstruction) patients can undergo percutaneous transhepatic decompression (PTC) with the possibility for future hybrid endoscopic-fluoroscopic interventions.23

Gangrenous cholecystitis is a manifestation of severe benign biliary disease where severe gallbladder infection is present without biliary tree obstruction. As implied in its name, these patients have severe distension and secondary infection of the gallbladder wall, leading to severe inflammation, ischemia, and necrosis and resulting in severe systemic infection.

Gangrenous cholecystitis can be challenging to manage. While the optimal management is minimally invasive cholecystectomy, severe inflammation can sometimes preclude safe laparoscopic removal of the gallbladder, increasing the likelihood of conversion to an open procedure. These patients are additionally at high risk of significant complications following cholecystectomy including iatrogenic common bile duct injury.24

PELVIC ABSCESS

Pelvic abscesses are defined as collection of infectious fluid in the pouch of Douglas, fallopian tube, ovary, or parametric tissue. It is usually seen as a complication after surgical procedures.25

Etiology

Pelvic abscesses can present as a complication from infections of the lower genital tract including pelvic inflammatory disease or as a complication after an operative procedure such as hysterectomies, laparotomies, cesarean sections, and induced abortions. They may also manifest secondary to cancers of the pelvic organs, trauma to the genital tract, complications due to Crohn disease, or diverticulitis.26 These could sometimes be complicated by intra-abdominal rupture, usually presenting as a life-threatening abdominal emergency with high morbidity and mortality.27

Evaluation

The clinical presentation is highly variable as the patients may present with high-grade fever, general malaise, nausea, vomiting, tachycardia, abdominal pain, vaginal discharge or bleeding, or change in bowel movements. Blood workup usually shows leukocytosis with elevated erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP).28 Complete physical examination including a thorough abdominal, vaginal, and rectal examination is essential to evaluate the characteristics of the abscess. Basic investigations should include complete blood cell count, blood cultures, exudate culture, and urine pregnancy test to rule out an intrauterine or ectopic pregnancy.

Various imaging techniques can be used to determine the size, location, and distribution of the pelvic abscess. Pelvic ultrasonography (USG) is commonly used as a first imaging modality in the women of reproductive age. It may reveal a collection of pus with varying internal echoes. Transvaginal USG is almost always superior to transabdominal USG.29

Other imaging modalities that are also used in the evaluation of pelvic abscess include CT and magnetic resonance imaging (MRI). They are particularly helpful in postoperative patients in whom USG is less likely to locate the abscess due to a collection of postoperative air, wound, or abundant bowel gas.30

Management

Patients with suspected pelvic abscess should be admitted and closely monitored for sepsis and rupture. Few patients may respond to conservative management alone including patients with no sign of sepsis and rupture, those who are hemodynamically stable, and those with relatively small size abscess. However, up to 25% of the patients fail to respond to conservative treatment and require surgical management.31

Empirical antimicrobial agents such as third-generation cephalosporin (eg, ceftriaxone) and metronidazole may be initiated to target polymicrobial flora. Other options include monotherapy with extended-spectrum penicillin (eg, piperacillin-tazobactam) and carbapenems such as meropenem.32 Parenteral antibiotics are usually continued for 24 to 48 hours after the patient becomes afebrile and then can be switched to oral antibiotics. The total duration of antibiotics is not well studied and varies on the basis of clinical improvement and source control.

Surgical drainage becomes necessary if the size of abscess if more than 8 cm or failure to respond to conservative management with antibiotics for 2 to 3 days.31

CT, MRI, or USG-guided drainage with antibiotics is the procedure of choice with high success rate in most of the patients.33 It has been shown to decrease the length of stay in hospital, has less morbidity, and requires no anesthesia when compared with laparoscopy.34 CT-guided percutaneous drainage is preferred for deep abscesses.34 Drainage or removal of abscess as much as possible is essential to prevent further surgical evacuation. All tissues or fluid should be sent for culture and histopathology. Drain is usually kept until the output from the drain diminishes and the patient improves clinically.

Endoscopic USG-guided drainage is sometimes opted when pelvic abscess is not amenable to percutaneous drainage.35 Few patients who have rupture of pelvic abscess, which is always a life-threatening emergency, require emergent surgery.

LIVER ABSCESS

Liver abscess is a pus-filled collection in the hepatic parenchyma that commonly develops due to direct injury to the liver, via hematogenous seeding or through extension from an intra-abdominal focus of infection.36 Most of the liver abscesses are from pyogenic and amoebic infections, but few can be caused by parasites and fungi.37

Pyogenic liver abscess

Pyogenic liver abscesses commonly develop following peritonitis secondary to leakage of intra-abdominal contents and then spread to the liver by portal circulation or via direct spread in the setting of biliary infection.

Epidemiology

In a study of 540 cases of intra-abdominal abscesses, pyogenic liver abscess accounted for 48% of visceral abscesses and 13% of intra-abdominal abscesses.38

Geographic and host factors play an important role, as underlying diabetes mellitus, hepatobiliary disease, liver transplant, and chronic granulomatous disease are all implicated as risk factors for the development of a liver abscess.39,40 Most pyogenic liver abscesses are polymicrobial. Potential pathogens include enteric gram-negative bacilli (Escherichia coli, Klebsiella pneumoniae), streptococci (specifically S pyogenes and S milleri group including S constellatus, S anginosus, and S intermedius), and Staphylococcus aureus and other gram-positive cocci in certain patient groups.41-43

Clinical presentation

Patients commonly present with fever and abdominal pain. A few proportions of the patients also have nausea, vomiting, anorexia, and malaise. Fever occurs in almost 90% of the patients, whereas abdominal symptoms present in half of the patients. Abdominal symptoms are usually localized to the right upper quadrant including pain and guarding. The absence of right upper-quadrant findings is not a sensitive finding and does not exclude liver abscess.44

Common laboratory abnormalities include elevated bilirubin, liver enzymes, and alkaline phosphatase. Few patients will also manifest leukocytosis and anemia.39,44,45

Diagnosis

The clinical presentation of fever with right upper-quadrant abdominal pain should prompt liver imaging. USG and CT with intravenous contrast are the 2 most used modalities. CT is more sensitive than USG to diagnose liver abscess.46

Blood cultures should be performed; they can be positive in up to half of cases.39,47 In critically ill patients, empiric antibiotic therapy should be started after obtaining the blood cultures. Serology and/or stool testing for Entamoeba histolytica should also be performed in patients who have epidemiologic risk factors for amoebic liver abscess such as travel from high endemic countries or in patients who do not have clear predisposing risk factors for pyogenic abscess.

When liver abscess is suspected, drainage or aspiration of the collections should be done as soon as possible for diagnostic as well as therapeutic reasons. Aspirate should be sent for Gram staining and culture. Cultures from existing drains should be avoided as shown by Everts et al,48 where cultures from percutaneous specimens correlated with cultures from drainage catheters in only half of the cases.

Management

Drainage is a key component of therapy and should be attempted whenever possible. CT or USG-guided percutaneous drainage is commonly used, but surgical drainage (either open or laparoscopic) is also used in select cases. Endoscopic USG-guided drainage is a new technique that has been shown to be safe and effective in difficult-to-access liver abscesses.49

For abscesses larger than 5 cm, catheter drainage is preferred over simple needle aspiration and has been shown to have a higher success rate.50 Larger abscesses (specially >10 cm) are at risk of treatment failure, though can still be successfully managed with catheter drainage.51 Patients with multiloculated abscesses traditionally undergo surgical drainage (open or laparoscopic), but some patients can be successfully managed by percutaneous drainage when collections are small and easily accessible.52

Empiric broad-spectrum parenteral antibiotics should be initiated ideally after aspiration of the abscess and should cover enteric gram-negative bacteria, streptococci, and anaerobes. Commonly used regimens include a third-generation cephalosporin plus metronidazole or piperacillin-tazobactam. Metronidazole can be added if E histolytica is suspected on the basis of risk factors. Antibiotic therapies are usually recommen-ded for 4 to 6 weeks.53

Chen et al54 showed in a study of 72 patients that acute respiratory failure and APACHE II score of more than 16 on the first day of ICU admission were significant prognostic factors.

Amoebic liver abscess

Amebic liver abscess is usually seen in migrants or travelers to endemic areas such as India, Africa, Mexico, and central and South America but can be seen in nonendemic areas due to sexual oral-anal contact.55,56

Patients usually present with right upper-quadrant pain and fever. Diarrhea occurs in less than a third of patients, whereas jaundice occurs in less than 10% of patients.57

USG usually shows cystic cavity in the liver and is commonly seen in the posterior right lobe of the liver. Most of the patients will have detectable antibodies, but it may be negative in the first 7 days.58 Needle aspiration or catheter drainage is not routinely performed but may be required if the cyst is more than 10 cm in diameter, at risk of rupture, or clinical worsening.59

It is recommended to start empiric treatment if clinical suspicion is high pending further diagnostic evaluation. Treatment consists of a tissue agent such as metronidazole or tinidazole and a luminal agent such as paromomycin to eliminate intraluminal cysts. High mortality can be seen in patients with increased bilirubin level, serum albumin less than 2.0 g/dL, large abscess cavity, multiple abscesses, and encephalopathy.60

OBSTRUCTIVE UROPATHY

Obstructive uropathy refers to the functional or structural alteration in the urinary tract that impedes urinary flow. Depending on the obstruction, subsequent backup of urine, unilateral or bilateral, results in hydronephrosis. Obstructive uropathy can be a potentially severe condition that results in significant morbidity and mortality. Therefore, early recognition and treatment of obstructive uropathy are paramount, as it is easily reversible if quickly corrected. The obstruction can present in many different ways, from minimal symptoms to fulminant sepsis. Most commonly, it presents as a combination of acute urinary retention, difficultly initiating micturition, or lower abdominal discomfort.

Etiology

Urinary tract obstruction can occur anywhere along the urinary tract-the cause of obstruction, in part, based upon the location of the obstruction. Obstruction within the kidney causes the dilatation of individual calyces. Etiologies of intrarenal obstruction include kidney stones, transitional cell carcinoma, and sloughed papillae.61

Obstruction at or distal to the renal pelvis causes hydronephrosis. Ureteral obstruction can be secondary to stones, transitional cell carcinoma, and external compression from enlarged lymph nodes, tumors, or retroperitoneal fibrosis. Similarly, a stent placed to relieve obstruction can at times result in obstruction, leading to recurrent hydronephrosis. Bladder outlet obstruction can result from prostate enlargement, posterior urethral valve, or neurogenic bladder.62

Etiologies of urinary tract obstruction vary with age as well. However, anatomic abnormalities are the underlying etiology for most cases in children. In comparison, calculi are the underlying etiology in young adults. In elderly patients, the primary causes are prostatic hypertrophy or carcinoma, calculi, and pelvic neoplasms.61-64 The potential causes are listed in the Table.

Table. Common Causes of Urinary Tract Obstruction

Clinical presentation

The clinical presentation of urinary tract obstruction depends upon the site of obstruction, duration of the obstruction, and degree of obstruction. It can be asymptomatic. Generally, the patient presents with 1 or more of the following symptoms and signs:

* Flank pain from upper urinary tract obstruction caused by distention of renal capsule or collecting system;

* Lower abdominal pain from bladder distention;

* Change in urine output;

* Macroscopic hematuria;

* Poor stream, terminal dribbling, or hesitancy from bladder outlet obstruction;

* Urgency, frequency, and urge incontinence from incomplete bladder emptying;

* Flank tenderness;

* A flank mass from enlarged hydronephrotic kidney; and

* Hypertension due to sodium and water retention from the abnormal release of renin.

Pain is frequently absent in the setting of acute obstruction and, when present, is suggestive of bladder distention, obstructing stone or mass, or secondary infection. Hydronephrosis alone is asymptomatic, and the presence of pain should prompt consideration of stones, infection, or papillary necrosis. Renal colic is seen with ureteral calculus or complete acute obstruction. While external ureteral compression leads to urinary tract obstruction, pain is absent because of the slowly progressive course of development of obstruction.

Normal urine output can be seen with urinary tract obstruction as well. Urine output is variable, which can range from anuria to polyuria. Polyuria results from tubular injury, which results in the impairment of tubules to retain salt and concentrate urine. Similarly, urethral obstruction causes bladder distention and present with overflow incontinence. It can result in abdominal distention, which one can appreciate with careful percussion of the lower abdomen.

Evaluation

A basic metabolic panel should be performed in patients with suspicion of obstructive uropathy, focusing on renal function and electrolytes. In general, obstruction of a single kidney, while the contralateral kidney is functional and not obstructed, does not lead to creatinine elevation. However, bilateral obstruction or unilateral obstruction in the setting of chronic kidney disease will result in elevated creatinine levels.65 Urinalysis is recommended to rule out urinary tract infections. The presence of microscopic hematuria can be suggestive of renal stones.

Early diagnosis of urinary tract obstruction is paramount since most cases are correctable and can prevent irreversible renal injury. USG is the preferred imaging test for most patients, given its widespread availability, safety, and relatively inexpensiveness. The positive predictive value is 70% in patients with clinical suspicion.66-68 The high negative predictive value of 98% in ruling out obstruction demonstrates the USG value in obstructive uropathy.66-69 Unilateral hydronephrosis raises suspicion of upper tract obstruction, whereas bilateral hydronephrosis is seen with pelvic or lower urinary tract pathology.70

In a setting where the obstructing stone is suspected, noncontrast CT is the initial study of choice.71,72 The characteristic features of an obstructing stone include flank pain, nausea, vomiting, dysuria, and hematuria. Risk factors include a prior personal or family history of nephrolithiasis. It is important to remember that CT scans expose patients to a significant radiation, dose-limiting their repetitive use.

MRI may be an alternative to CT since it does not expose patients to radiation.71 However, stones are poorly visualized by MRI. In addition, gadolinium contrast required for MRI is avoided in patients with impaired renal function as there is a risk of developing nephrogenic systemic fibrosis after exposure to gadolinium contrast.73

Management

Management of urinary tract obstruction depends on the etiology of obstruction, location of the obstruction, degree of renal impairment, and imaging findings. Acute kidney injury resulting from urinary obstruction will resolve once the obstruction is treated promptly.62,74 Local expertise and resources dictate management in practice.

Lower urinary tract obstruction is rapidly relieved by placing the urinary catheter, while more definitive treatment is done on the basis of the underlying etiology. The initial attempt usually occurs with a 16 or 18 Fr Foley catheter.75 If there is no success with initial attempts, the next step would be a trial of urethral catheterization using a coude tip Foley catheter but may require higher-level intervention if attempts are unsuccessful.75-78 While rare, suprapubic catheterization or cystostomy may be required when urethral catheterization is unsuccessful or not feasible.76-78

Obstruction secondary to prostatic disease would need further workup to rule out malignancy. Prostate treatment can be medical and surgical, guided on the basis of individual factors, disease characteristics, and local expertise.

Acute obstruction can be associated with infection and sepsis that needs urgent decompression.62,74 Urgent decompression can be accomplished with nephrostomy tube insertion or by ureteral stent placement.79,80 If the underlying etiology is urolithiasis, stone removal is done once the infection is adequately controlled and treated. Stone size, location, and composition play a crucial role in deciding the best modality for stone removal.

Once the obstruction has been relieved, postobstructive diuresis can develop, which results in the excretion of water and electrolytes; since there is an acquired tubular dysfunction, which takes days to a week to recover, a considerable amount of electrolytes may be lost inappropriately in the urine.81 Therefore, careful monitoring of serum electrolytes is indicated to ensure complications do not develop as a result.

FOREIGN BODY ASPIRATION

Foreign body aspiration is a frequently encountered problem worldwide and can be a life-threatening emergency. Aspirated and ingested foreign bodies present diagnostic and therapeutic challenges. If the foreign body is large enough to cause complete airway obstruction, this results in compromised airway, leading to asphyxia. Partial obstruction of passage into the tracheobronchial tree beyond the carina can result in less severe signs, symptoms, including recurrent infections, and discomfort, or the patient may remain asymptomatic.

Epidemiology

Foreign body aspiration is more common in children than in adults. Patients younger than 15 years constitute 80% of the cases, with the remaining 20% presenting in those older than 15 years. Death from foreign body aspiration presents a bimodal pattern, with peaks at ages less than 1 year and greater than 75 years.82 Over a 20-year analysis of fatalities by Mittleman and Wetli83 determined that most events occurred at home (41%), followed by in restaurants (29%) and then health care facilities including nursing homes or mental institutions (14%).

Pathogenesis

In adults, foreign body aspiration results from a failure of the airway projective mechanism and is primarily seen in the seventh decade of life.84-86 Factors that are contributory include the following:

* Alcohol intoxication;

* Sedative or hypnotic drug use;

* Poor dentition;

* Mental retardation;

* Parkinson disease;

* Primary neurologic disorders with impairment of swallowing or mental status;

* Trauma with loss of consciousness;

* Seizure; and

* General anesthesia.

In children, food particles, particularly nuts and seeds, account for most foreign body aspiration. Other materials include coins, toys, and balloons. However, in adults, the included objects are highly variable, ranging from organic to inorganic materials.

Inorganic material includes, but not limited to, aspiration of dental debris, prostheses, or appliances, which can complicate dental procedures or facial trauma.87-89 In addition, there can be the accidental aspiration of nails or pin during work activities in middle-aged adults. Organic materials include frequently aspirated food due to incomplete chewing or impaired swallowing function.90-93

Clinical presentation

The clinical presentation of foreign body aspiration depends on the location of the obstruction, degree of obstruction, and length of time that the foreign body has been in the airway. A large object that completely occludes the larynx will present with acute onset of choking, severe coughing, and gagging. Rarely, the patient may not be able to speak and presents with cyanosis. Most of the cases in the adults are often subtle or silent. Distal obstruction of the lower airway involving the bronchi results in chronic cough as presenting symptom. Only a small percentage of patients present with the classic triad of wheezing, choking, and cough.94,95

In 80% of all cases, patients present with acute or chronic cough; other associated symptoms include wheeze, fever, hemoptysis, chest pain, and foul-smelling sputum. Most patients do not recall a history of choking or an aspiration event, which frequently results in a delay in diagnosis.96-99 The most common site of impaction is the right lower-lobe bronchus because it is more vertically continuous with the trachea and larger in diameter.100,101 Because of the lack of specificity of the symptoms, adult airway foreign bodies often are misdiagnosed and can be delayed for months to years. Delayed complications to foreign body aspiration include bronchial stenosis, recurrent pneumonia, pneumothorax, recurrent hemoptysis, and chronic lung disease.102

Evaluation

In a case of suspected acute asphyxiation of a foreign body, imaging should not delay intervention, but imaging is indicated in stable patients. A chest radiograph is of limited value as the diagnosis can only be made in a small percentage of patients with a radiopaque aspirated foreign body. Most foreign bodies are radiolucent and not easily identified on plain film radiograps. Indirect, subtle signs such as atelectasis, pulmonary infiltration, and air trapping may suggest a foreign body.103 Flexible bronchoscopy is the gold standard in identifying the foreign airway body. Visual airway inspection is recommended if clinical suspicion is high, irrespective of radiographic findings. Flexible bronchoscopy is often the diagnostic procedure of choice in the non-life-threatening foreign body aspiration, given its widespread availability, visualization capabilities allowing precise localization and facilitating the interventional possibilities necessary for retrieval.

Management

In acute upper airway asphyxiation with a conscious patient, there are data supporting first aid maneuvers, including chest thrusts, back blows, blind finger sweeps, and abdominal thrust to relieve the foreign body obstruction.

In life-threatening asphyxiation, where a foreign body completely obstructs the upper airway involving the glottis, supraglottis, or trachea, the initial focus must be on the oxygenating patient and securing the airway. Initial attempts include bag-mask ventilation and endotracheal intubation. If an attempt is unsuccessful, emergent cricothyrotomy or tracheotomy is required if the foreign body is above the vocal cords. Once the airway is secured and the patient has been stabilized, immediate inspection of the oropharynx is undertaken. The foreign body lodged in the oropharynx can be removed using Magill forceps using direct laryngoscopy.

In patients with non-life-threatening foreign body aspiration, flexible bronchoscopy is often the initial procedure of choice. The success rate of flexible bronchoscopic extraction ranges from 55% to 80%.100-105 The oral approach is preferred, allowing easy removal through the mouth rather than being pulled through the nasal passage. In addition, flexible bronchoscopy allows the procedure to be done under conscious sedation, unlike rigid bronchoscopy, which requires general anesthesia. Currently available tools that can be used for extraction include forceps, fishnet baskets, snares, balloon-tipped catheters, magnet-tipped probes, and cryoprobes. Choice of retrieval tool varies with the nature of the foreign body, size, shape, and location. During the retrieval, care should be taken to ensure the foreign body is not pushed distally within the bronchoscope or grasping device. Once the foreign body is removed, the bronchoscope is reintroduced, and airways are carefully reexamined to rule out another foreign body or residual fragments.106

NECROTIZING SOFT-TISSUE INFECTIONS

Necrotizing soft tissue infections (NSTIs) commonly affect the deep layers of adipose tissue, fascia, or muscle. NSTIs are caused by toxin-producing bacteria and result in significant local tissue destruction with rapid progression of disease. Early diagnosis and treatment are vital for favorable outcomes. Hence, a high index of suspicion to rapidly diagnose NSTIs is imperative.107,108

Epidemiology

The incidence has been increasing, which may be a result of greater awareness of this condition leading to earlier diagnosis and reporting.109 NSTIs can occur at any age or gender, but higher rates have been seen in obese, diabetic, and immunocompromised patients, person affected with alcoholism, and those with peripheral vascular disease.110

Etiology

Inoculation of the pathogen into the subcutaneous tissue initiates the cascade of infection and inflammation. Inoculations can occur from trauma, intravenous drug use and insulin injections, skin ulcers, animal and insect bites, fistulas, surgical complications, and percutaneous catheter insertion. In some instances, the source of entry may remain unclear or unidentified.107 Fournier gangrene is NSTI of the perineum and genitalia that occurs from trauma, urinary tract infections, surgery, or other instrumentation. Diabetes remains an important risk factor for NSTIs of the perineum, lower extremities, and head and neck area.111

Classification

Giuliano and colleagues112 first described the classification of NSTIs as one of 2 bacteriologic classes.

Type I NSTIs

Type I infections are polymicrobial with gram-positive cocci, gram-negative rods, and anaerobes. Patients are older, with multiple comorbidities, and often with no antecedent trauma.107,109 Clostridial infections, a subtype of type of type I NSTIs, traditionally known as gas gangrene, present with rapid onset of severe pain, often out of proportion to the clinical examination with foul-smelling wound drainage and at times with woody induration of nearby tissue with associated tissue crepitus.113

Type II NSTIs

Type II infections include group A beta-hemolytic streptococci (GAS), either alone or in combination with staphylococci. Patients are usually younger, healthier, and have a history of trauma, surgery, or intravenous drug use.114

Monomicrobial NSTIs can also be caused by gram-negative marine organisms, commonly Vibrio vulnificus, and is classified by some authors as type III NSTIs. There can be early significant systemic toxicity, multiorgan failure, and cardiovascular collapse.115

Clinical presentation and diagnosis

Clinical presentation varies depending on the cause and hence type of NSTIs. Induration, edema beyond the area of skin, and pain out of proportion to examination are some common symptoms. Classic signs include erythema, swelling, pain beyond the margins of swelling, and fever. Presence of bullae, skin ecchymosis, crepitus, and gas in the tissue and cutaneous anesthesia are rare but should prompt immediate surgical exploration. Usual laboratory workup shows leukocytosis and elevated CRP, creatinine, and glucose levels. There is limited role for imaging in a suspected NSTI, but CT is more sensitive than plain radiography. In the setting of high clinical suspicion, gold standard for diagnosis remains operative exploration.107

Management

Early and wide removal of infected and necrotic tissue with radical surgical debridement is the mainstay of treatment.116 Broad-spectrum antimicrobial therapy should be initiated in all suspected NSTI cases. Empiric therapy includes coverage for gram-positive, gram-negative, and anaerobic pathogens. One such regimen used is vancomycin, piperacillin-tazobactam, and clindamycin. Clindamycin has been shown to decrease toxin production by clostridial species and superantigen production by streptococcal species. The antimicrobial regimen is then narrowed on the basis of the operative debridement, culture results, and clinical improvement.107,117

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