Cardiogenic shock differential diagnosis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: João André Alves Silva, M.D. [2] Syed Musadiq Ali M.B.B.S.[3] Ramyar Ghandriz MD[4]

Overview

Shock is a clinical syndrome resulting from the hypoperfusion of the tissues. Regardless of the underlying cause, this hypoperfusion leads to the failure to meet tissues' nutritional and oxygen needs, causing cellular dysfunction. The affected tissues lead to the production and release of inflammatory mediators that will further jeopardize perfusion through changes in the vasculature. The results of these changes are organ failure and death if treatment in not timely applied. According to the underlying cause, there will be different types of shock, which will have similar presentations. It is mandatory to determine the underlying cause of the condition so that proper treatment may be started. Cardiogenic shock is a clinical condition, defined as a state of systemic hypoperfusion originated in cardiac failure, in the presence of adequate intravascular volume, typically followed by hypotension, which leads to insufficient ability to meet oxygen and nutrient demands of organs and other peripheral tissues. It may range from mild to severe hypoperfusion and may be defined in terms of hemodynamic parameters, which according to most studies, means a state in which systolic blood pressure is persistently < 90 mm Hg or < 80 mm Hg, for longer than 1 hour, with adequate or elevated left and right ventricular filling pressures that does not respond to isolated fluid administration, is secondary to cardiac failure and occurs with signs of hypoperfusion (oliguria, cool extremities, cyanosis and altered mental status) or a cardiac index of < 2.2 L/min/m² (on inotropic, vasopressor or circulatory device support) or < 1.8-2.2 L/min/m² (off support) and pulmonary artery wedge pressure > 18 mm Hg.

Differential Diagnosis

Depending on the author and the source used there will be different ways of organizing the types of shock. Sometimes it might be difficult to differentiate, from the clinical standpoint, two types of shock since components of each type may combine in a single patient. The clinical presentation of shock is usually the result of a complexity of processes, such as the sympathetic and endocrine responses to hypoperfusion, along with manifestations of organ failure. Patients who present with signs and symptoms of hypoperfusion following a diagnosed or suspected myocardial infarction, are commonly suffering a cardiogenic shock as a complication of the MI. However, other clinical scenarios, not related to acute MI, may present similarly:

• Hypovolemic shock

• More than a simple loss of intravascular volume, hypovolemic shock is a dynamic process in which the responses to the initial insult, and the period of time during which they are in practice, will dictate the response to treatment and therefore the outcome. Several causes may be in the origin of this type of shock, including: hemorrhage, dehydration, GI or urinary losses and severe venodilation (in the setting of other conditions). There is a relationship between the clinical status of the patient and the amount of circulating blood volume, the signs may include pallor, cool extremities, tachycardia and tachypnea, oliguria and decreased consciousness. Compensatory mechanisms are responsible for tolerating initial blood loss, however they begin to fail after about 20-25% of blood has been lost. This tolerance will be dictated mostly by the previous cardiac reserve of the patient, along with the velocity of loss of intravascular volume.
• When comparing hypovolemic and cardiogenic shock (most commonly complicating acute-MI) some specific clinical signs of shock will be similar, however, others will be different, particularly signs of CHF, such as the presence of distended jugular and peripheral veins, presence of an S3 sound and pulmonary edema on the cardiogenic type.
• When comparing hemodynamic data, similarities include: decreased cardiac index, stroke volume index, cardiac output, mixed venous oxygen saturation and increased difference in arteriovenous O₂ saturation and SVR.

Differences to be noted include:

<math>\mbox{Shock index} = \frac{heart\ rate}{systolic\ blood\ pressure}</math>

Other measures include: decreased ventricular preload, ventricular diastolic volumes and pressures, pulmonary wedge pressure and central venous pressure.

• When treating hypovolemic shock it's mandatory to rule out cardiogenic cause because part of the treatment for hypovolemic shock, urgent intravascular volume replacement, may further jeopardize the cardiac condition in the cardiogenic form.

• Obstructive shock

• This form of shock results from an obstruction to the flow of blood through the cardiovascular system, including the vessels and the heart. Therefore, different causes may give rise to this condition, such as: tension pneumothorax, pulmonary emboli, pericardial tamponade and constrictive pericarditis. As in other types of shock, the clinical response will be heavily dictated by the timespan during which the insult develops and urgent therapy must be applied.
• To evaluate the hemodynamics of obstructive shock it is important to know the underlying etiology of the shock, since different causes will present with different hemodynamic values. One example of cause of obstructive shock is cardiac tamponade, which, similarly to the cardiogenic form, will likely present with: decreased cardiac index, stroke volume, stroke work, mixed venous oxygen saturation and increased difference in arteriovenous O₂ saturation, right and left ventricular diastolic pressures, pulmonary artery diastolic pressure, serum lactate and CVP. Other causes may be observed on the table below.

• Distributive shock

• The hallmark of this form of shock is the decrease of peripheral resistance. This may be present in a series of conditions that may lead to distributive shock, such as: sepsis, anaphylaxis, toxic shock syndrome and adrenal crisis.
• When compared to cardiogenic shock it presents with similarities, such as: decreased cardiac index, left and right ventricular stroke work and increased serum lactate. The differences reside in: overall decreased of SVR, which after fluid resuscitation may become elevated, ventricular filling pressure, difference in arteriovenous O₂ saturation and increase of mixed venous oxygen saturation. It is important to note that, unlike cardiogenic and other types of shock, in the distributive kind there is an increase in venous oxygen saturation which, despite the increased O₂ demand, might be due to the increased total body perfusion, that is responsible for diminishing the effectiveness of individual tissue perfusion.

Classification of shock based on hemodynamic parameters. (CO, cardiac output; CVP; central venous pressure; PAD, pulmonary artery diastolic pressure; PAS, pulmonary artery systolic pressure; RVD, right ventricular diastolic pressure; RVS, right ventricular systolic pressure; SVO2, systemic venous oxygen saturation; SVR, systemic vascular resistance.)

Type of Shock	Etiology	CO	SVR	PCWP	CVP	SVO2	RVS	RVD	PAS	PAD
Cardiogenic	Acute Ventricular Septal Defect	↓↓	↑	N — ↑	↑↑	↑ — ↑↑	N — ↑	↑	N — ↑	N — ↑
	Acute Mitral Regurgitation	↓↓	↑	↑↑	↑ — ↑↑	↓	↑	N — ↑	↑	↑
	Myocardial Dysfunction	↓↓	↑	↑↑	↑↑	↓	N — ↑	N — ↑	N — ↑	↑
	Right Ventricular Infarction	↓↓	↑	N — ↓	↑↑	↓	↓ — ↑	↑	↓ — ↑	↓ — ↑
Obstructive	Pulmonary Embolism	↓↓	↑	N — ↓	↑↑	↓	↓ — ↑	↑	↓ — ↑	↓ — ↑
	Cardiac Tamponade	↓ — ↓↓	↑	↑↑	↑↑	↓	N — ↑	↑	N — ↑	N — ↑
Distributive	Septic Shock	N — ↑↑	↓ — ↓↓	N — ↓	N — ↓	↑ — ↑↑	N — ↓	N — ↓	↓	↓
	Anaphylactic Shock	N — ↑↑	↓ — ↓↓	N — ↓	N — ↓	↑ — ↑↑	N — ↓	N — ↓	↓	↓
Hypovolemic	Volume Depletion	↓↓	↑	↓↓	↓↓	↓	N — ↓	N — ↓	↓	↓

The following table outlines the major differential diagnoses of Shock on the basis of clinical manifestations..

Abbreviations: ABG (arterial blood gas); ACE (angiotensin converting enzyme); BMI (body mass index); CBC (complete blood count); CSF (cerebrospinal fluid); CXR (chest X-ray); ECG (electrocardiogram); FEF (forced expiratory flow rate); FEV1 (forced expiratory volume); FVC (forced vital capacity); JVD (jugular vein distention); MCV (mean corpuscular volume); Plt (platelet); RV (residual volume); SIADH (syndrome of inappropriate antidiuretic hormone); TSH (thyroid stimulating hormone); Vt (tidal volume); WBC (white blood cell); Coronary CT angiography (CCTA); multidetector row scanners (MDCT); Cardiovascular magnetic resonance — CMRI; Myocardial perfusion imaging (MPI); single-photon emission CT (SPECT); Positron emission tomography (PET) scanning; Magnetic resonance (MR) angiography, Computed tomographic (CT) angiography, and Transesophageal echocardiography (TEE), late gadolinium enhancement (LGE); right ventricular hypertrophy (RVH), right atrial enlargement (RAE), functional tricuspid regurgitation (TR), Pulmonary artery systolic pressure (PASP; adenosine deaminase (ADA); Serum amyloid A (SAA), soluble interleukin-2 receptor (sIL2R); High-resolution CT (HRCT) scanning

Differentials on the basis of Etiology	Disease	Clinical manifestations										Diagnosis
		Symptoms								Risk factors	Physical exam	Lab Findings	EKG	Imaging	Gold standard
		Onset	Duration	Quality of Pain	Cough	Fever	Dyspnea	Weight loss	Associated Features
	Myocardial Infarction	Acute	Commonly > 20 minutes	Same as stable angina but often more severe	-	-	+	-	Nausea and vomiting Diaphoresis Presyncope Palpitations Lateral displacement of the apical impulse	Dyslipidemia, hypertension, smoking, family history of premature disease, and diabetes	Hypotension Tachycardia S4 gallop Paradoxical splitting of S2 Mitral regurgitation murmur	Elevated cardiac enzymes ↑B-Type Natriuretic Peptide	ST elevation MI (STEMI) Non-ST elevation MI (NSTEMI) or Non Q wave	Echocardiography: ↓ EF CCTA: Coronory artery stenosis CMRI: Coronory vessels stenosis MPI on SPECT or PET scanning: Decreased myocardial perfusion.	CCTA combined with MPI
Cardiac
	Aortic Dissection	Sudden severe progressive pain (common) or chronic (rare)	Variable	Tearing, ripping sensation, knife like	-	-	+	-	Focal neurologic deficit Hypotension	Hypertension Genetically mediated collagen disorders Preexisting aortic aneurysm Bicuspid aortic valve Aortic coarctation Turner syndrome Vasculitis (giant cell arteritis, Takayasu arteritis, rheumatoid arthritis, syphilitic aortitis)	Pulse deficit New diastolic murmur Diastolic decrescendo murmur Focal neurologic deficit Hypotension	D-dimer <500 ng/mL rules out aortic dissection ↑Soluble ST2 (sST2) Measurements of soluble elastin fragments, smooth muscle myosin heavy chain, high-sensitivity C-reactive protein, fibrinogen, and fibrillin fragments	Nonspecific ST and T wave changes	CXR: Mediastinal and/or aortic widening CTA: A compressed true lumen MRA: Detects differential flow between the true and false lumens, widening of the aorta with a thickened wall TEE: Intimal dissection flaps, true and false lumens, thrombosis in the false lumen Aortography: Distortion of the normal contrast column, Flow reversal or stasis into a false channel, Failure of major branches to fill, and Aortic valvular regurgitation	CT angiography Digital subtraction aortography (if high suspicion)
	Aortic intramural hematoma	Sudden severe progressive pain (common) or chronic (rare)	Variable	Tearing, ripping sensation, knife like	-	-	+	-	Focal neurologic deficit Hypotension	Hypertension Genetically mediated collagen disorders Preexisting aortic aneurysm Bicuspid aortic valve Aortic coarctation Turner syndrome Vasculitis (giant cell arteritis, Takayasu arteritis, rheumatoid arthritis, syphilitic aortitis)	Pulse deficit New diastolic murmur Diastolic decrescendo murmur Focal neurologic deficit Hypotension	D-dimer <500 ng/mL rules out aortic dissection ↑Soluble ST2 (sST2) Measurements of soluble elastin fragments, smooth muscle myosin heavy chain, high-sensitivity C-reactive protein, fibrinogen, and fibrillin fragments	Nonspecific ST and T wave changes	CXR: Mediastinal and/or aortic widening CTA: A compressed true lumen MRA: Detects differential flow between the true and false lumens, widening of the aorta with a thickened wall TEE: Intimal dissection flaps, true and false lumens, thrombosis in the false lumen Aortography: Distortion of the normal contrast column, Flow reversal or stasis into a false channel, Failure of major branches to fill, and Aortic valvular regurgitation	CT angiography Digital subtraction aortography (if high suspicion)
	Penetrating atherosclerotic aortic ulcer	Sudden severe pain	Variable	Tearing, ripping sensation, knife like	-	-	+	-	Hypotension Back pain Hypovolemic shock	Hypertension Smoking Hyperlipidemia Atherosclerosis Male gender Older age Bicuspid aortic valve Prior aortic surgery Prior aortic dilatation	Hypotension	_	_	CXR: Mediastinal and/or aortic widening, diffuse or focal enlargement of thoracic descending aorta, pleural effusion, and deviated trachea CTA: Presence of false aneurysm	CT angiography Contrast-enhanced CT scan
	Pericardial Tamponade	Acute or subacute	May last for hours to days	Sharp and stabbing retrosternal pain	+/-	+	+	-	Pulsus paradoxus Pericardial rub	HIV TB Immunosuppression Acute trauma	Kussmaul sign Beck triad Pulsus paradoxus	Creatine kinase and isoenzymes Abnormal LFTs Antinuclear antibody assay, erythrocyte sedimentation rate and rheumatoid factor HIV testing	EKG findings: Sinus tachycardia Low QRS voltage Electrical alternans	CXR: enlarged cardiac silhouette with clear lung fields Echocardiography: Chamber collapse, Respiratory variation in volumes and flows, IVC plethora Swan-Ganz Catheterization: Equilibration of average intracardiac diastolic pressures (usually between 10 and 30 mmHg)	Echocardiography
	Myocarditis	Acute or subacute	Variable	Sharp & localized retrosternal pain reflects associated pericarditis	+/-	+	+	-	Heart failure Sudden cardiac death Arrythmias	Ischemic heart disease Valvular heart disease	S3 and S4 gallop Cardiac murmurs Pericardial friction rub	Serum cardiac troponin levels ↑ BNP or NT-proBNP level	Nonspecific ST changes, single atrial or ventricular ectopic beats, complex ventricular arrhythmias	CXR: Normal to enlarged with or without pulmonary vascular congestion and pleural effusions Echo: Left ventricular dilation, changes in left ventricular geometry (eg, development of a more spheroid shape), and wall motion abnormalities CMR: T1 and T2 signal intensity consistent with edema, presence of LGE consistent with necrosis or scar Radionuclide ventriculography: ↓ EF Cardiac catheterization: Assessment of hemodynamic status	Endomyocardial biopsy
	Hypertrophic cardiomyopathy	Acute or subacute	Variable	Typical or atypical chest pain	-	-	+	-	HF Arrhythmias Syncope Acute hemodynamic collapse	Positive family history of sudden cardiac death Genetic mutation	S4 Systolic murmurs LV apical impulse Brisk carotid pulse ↑ JVP A parasternal lift	Non-specific	Prominent abnormal Q waves P wave abnormalities Left axis deviation Deeply inverted T waves	Echocardiography: LV hypertrophy Systolic anterior motion of the mitral valve, LVOT obstruction  Cardiac catheterization Pressure gradient Augmentation of the gradient Aortic pressure Left ventricular pressure Left atrial or pulmonary capillary wedge pressure Coronary angiography Obstructive epicardial coronary artery disease Genetic testing for HCM: Sarcomere mutation in an athlete with a maximal LV wall thickness in the "grey zone"	Genetic testing for HCM
	Stress (takotsubo) Cardiomyopathy	Acute	Commonly > 20 minutes	Substernal heaviness or tightness	-	-	+	-	Setting of physical or emotional stress or critical illness	Stress	Murmurs and rales may be present on auscultation in the setting of acute pulmonary edema	Catecholamines transiently elevated ↑TnT level ↑BNP level	ST segment elevation ST depression QT interval prolongation, T wave inversion, abnormal Q waves	Radionuclide myocardial perfusion imaging: Transient perfusion abnormalities in the left ventricular apex	Ventriculography and invasive coronary angiography
	Aortic Stenosis	Acute, recurrent episodes of angina	2-10 minutes	Heaviness/pressure/ tightness/squeezing/ burning (Levine's sign) Retrosternal	-	-	+	-	Dyspnea and decreased exercise tolerance Dizziness and syncope Angina pectoris	HTN Old age	S2 is soft, single and paradoxically split A2 delayed and tends to occur simultaneously with P2 Aortic ejection click Fourth heart sound (S4) can also be heard Crescendo–decrescendo murmur	Schistiocytes on peripheral blood smear	Non specific (the voltage of the QRS complex is increased showing the presence of left ventricular hypertrophy)	Echocardiography: aortic leaflets thickened and calcified, ↑ pulmonary artery pressure) CMR: Myocardial fibrosis, evaluation of aortic anatomy and size MDCT: Degree of aortic valve calcification PET: Measures active mineralization which correlates with stenosis severity	Echocardiography
	Heart Failure	Subacute or chronic	Variable	Dull Left sided chest pain	+	+/-	+	+	Orthopnea Peripheral edema Hemoptysis	Dyslipidemia, hypertension, smoking, family history of premature disease, and diabetes	S3 Elevated JVP Peripheral edema	Hyponatremia Hypoalbuminemia ↑ Serum brain natriuretic peptide (BNP) or NT-proBNP level A mild elevation in serum bilirubin (total bilirubin <3 mg/dL)	EKG findings are specific according to each cause of heart failure Q waves, ST and T wave abnormalities in patients with prior MI New onset arrhythmias (atrial fibrillation and ventricular tachycardia)	CXR: Cardiomegaly Echocardiography: ↓ EF Right heart catheterization: Pulmonary capillary wedge pressure >20 mmHg, right atrial pressure ≥12 mmHg) and/or decreased cardiac index (≤2.2 L/min/m2	Echocardiography
Differentials on the basis of Etiology	Disease	Clinical manifestations										Diagnosis
		Symptoms								Risk factors	Physical exam	Lab Findings	EKG	Imaging	Gold standard
		Onset	Duration	Quality of Pain	Cough	Fever	Dyspnea	Weight loss	Associated Features
Pulmonary	Pulmonary Embolism	Acute	May last minutes to hours	Sharp or knifelike or pleuritic pain Localized to side of lesion	+	+/-	+	-	Hemoptysis History of venous thromboembolism or coagulation abnormalities.	Hormone replacement therapy Cancer Oral contraceptive pills Stroke  Pregnancy Postpartum  Prior history of VTE Thrombophilia	S3 or S4 gallop Low grade fever Tachycardia Tachypnea Hypoxia	↑D-dimer ≥500 ng/mL Arterial blood gases (Respiratory alkalosis) ↑Troponin levels Hypercoagulation workup	Tachycardia and nonspecific ST-segment and T-wave changes (70 percent) S1Q3T3 pattern New right bundle branch block Inferior Q-waves (leads II, III, and aVF)	Duplex Ultrasonography: DVT CXR: Westermark sign, Hampton hump, Palla's sign Echocardiography: RV dilation (ratio of apical 4-chamber RV diameter to left ventricle (LV) diameter > 0.9) RV systolic dysfunction Ventilation-Perfusion Scanning: High probability	CT pulmonary angiography
	Spontaneous Pneumothorax	Acute	May last minutes to hours	Sharp Localized pleuritic	-	-	+	-	Respiratory distress Tachypnea  Asymmetric lung expansion Hyperresonance on percussion Decreased tactile fremitus Tachycardia Cardiac apical displacement	Smoking Positive family history Marfan syndrome Homocystinuria Thoracic endometriosis.	Decreased breath sounds on involved side Lung sounds transmitted from the unaffected hemithorax are minimal with auscultation at the midaxillary line Adventitious lung sounds (crackles, wheeze; an ipsilateral finding) Pulsus paradoxus	Respiratory alkalosis on ABGs	Rightward shift in the mean electrical axis Loss of precordial R waves Diminution of the QRS voltage Precordial T wave inversions	CXR: White visceral pleural line on the chest radiograph CT: small amounts of intrapleural gas, atypical collections of pleural gas, and loculated pneumothoraces	CT scan
	Tension Pneumothorax	Acute	May last minutes to hours	Sharp Pleuritic	-	-	+	-	Hypotension Jugular venous distention Respiratory distress	Trauma	Decreased breath sounds on involved side Lung sounds transmitted from the unaffected hemithorax are minimal with auscultation at the midaxillary line Adventitious lung sounds (crackles, wheeze; an ipsilateral finding) Pulsus paradoxus	Respiratory alkalosis on ABGs	Significant elevation of the ST-T segment from leads V1 to V4	CXR: A distinct shift of the mediastinum to the contralateral side, collapse of the ipsilateral lung, and flattening or inversion of the ipsilateral hemidiaphragm	CT scan
	Pleural Effusion	Acute or subacute or chronic	Variable	Dull Pleuritic pain	+	+/-	+	+/-	Increasing lower extremity edema Orthopnea Paroxysmal nocturnal dyspnea Night sweats Hemoptysis	Pneumonia	Diminished or inaudible breath sounds Pleural friction rub Egophony (known as "E-to-A" changes)	Pleural fluid LDH levels above 1000 IU/L Nucleated cells - Lymphocytosis - Eosinophilia - Mesothelial cells Pleural fluid culture and cytology Pleural fluid antinuclear antibody and rheumatoid factor	Typically not indicated	Chest X Ray: Pleural fluid on one or both sides Computerized tomography (CT) scan: Detects small pleural effusions, ie, less than 10 mL and possibly as little as 2 mL of liquid in the pleural space, Thickening of the visceral and parietal pleura  MRI: Characterize the content of pleural effusions	Computed tomography
	Acute chest syndrome (Sickle cell anemia)	Acute	May last minutes to hours	Chest tightness	+	+/-	+	-	Sickle cell anemia Vaso-occlusive crisis Pain crises	↑ WBC ↑ Hb levels ↓ fetal hemoglobin levels Smoking Vaso-occlusive pain events	Systolic murmur may be heard over the entire precordium	↑Erythrocyte sedimentation rate Peripheral blood smears: Schistiocytes ↑ Reticulocyte count	EKG typically not indicated	Plain radiography of the extremities: Avascular necrosis	---
Differentials on the basis of Etiology	Disease	Clinical manifestations										Diagnosis
		Symptoms								Risk factors	Physical exam	Lab Findings	EKG	Imaging	Gold standard
		Onset	Duration	Quality of Pain	Cough	Fever	Dyspnea	Weight loss	Associated Features
Gastrointestinal	Perforated Peptic Ulcer	Acute	Minutes to hours (gastroesophageal reflux) Prolonged (peptic ulcer) 5 to 60 minutes	Burning Substernal Epigastric	+/-	-	-	+/-	Visceral, substernal, worse with recumbency, no radiation, relief with food, antacids Hematemesis or melena resulting from gastrointestinal bleeding Dyspepsia	Prolonged NSAIDs intake Smoking Alcohol abuse Spicy foods H-pylori infection	Not any auscultatory findings associated with this disease Enamel erosion or other dental manifestations	↑Serum Gastrin Level Secretin Stimulation Test H-Pylori testing	EKG usually normal but may show T wave inversions in leads V2 through V4 consistent with myocardial ischemia in patients with peptic ulcer perforation	Upper Gastrointestinal Endoscopy: Biopsy Esophageal Manometry: To exclude an esophageal motility disorder Esophageal impedance pH testing: Monitors esophageal pH	Upper Gastrointestinal Endoscopy
	Esophagitis	Acute	Variable	Burning Epigastric	+	+	-	+/-	Heartburn Abdominal pain	HIV Immunosuppression	No auscultatory finding	Troponin or other cardiac markers Leukopenia ↓CD4 count Human immunodeficiency virus (HIV) test	ECG is done to rule out acute coronary syndrome	Double-contrast esophageal barium study (esophagography) Endoscopy: Biopsy	Endoscopy
	Esophageal Perforation	Acute	Minutes to hours	Burning Upper abdominal	-	+/-	+	-	Eating disorders such as bulimia Repeated episodes of retching and vomiting with either recent excessive dietary or alcohol intake Subcutaneous emphysema	Instrumentation/surgery Penetrating or blunt trauma Medications, other ingestions, foreign body Violent retching/vomiting Hernia/intestinal volvulus/obstruction Inflammatory bowel disease Appendicitis Peptic ulcer disease	Mild tachycardia or hypothermia Hamman crunch (crackling sound upon chest auscultation occurs due to pneumomediastinum)	↑Serum amylase ↑C-reactive protein levels	EKG may be indicated to assess for myocardial ischemia due to acute gastrointestinal bleeding, especially if there is coexisting:Cardiovascular disease, significant anemia and advanced age	Plain chest films or chest CT: Pneumomediastinum, Free air under the diaphragm, •Pleural effusion •Pneumothorax (Macklin effect).   •Subcutaneous emphysema Plain abdominal films (or abdominal CT scout film):The appearance of pneumoperitoneum -Free air under the diaphragm -Cupola sign (inverted cup) -Rigler sign (double-wall sign) -Psoas sign -Urachus sign	Confirmed by water-soluble contrast esophagram
	Mediastinitis	Acute, Chronic	Variable	Retrosternal irritation	+/-	+	+	-	Nonspecific	Infection Esophageal perforation Post operative complication	Dysphagia Dysphonia Stridor Hamman sign	Positive organisms in sternal culture Leukocytosis Positive blood cultures	Diffuse ST elevation	CT: Localize the infection and extent of spread MRI: Assesses vascular involvement and complications	CT scan
	Pancreatitis	Acute, Chronic	Variable	Epigastric Upper left side of the abdomen Pressure like	-	+	+	+/-	Primary cirrhosis Primary sclerosing cholangitis Cystic fibrosis Autoimmune diseases	Alcohol abuse Smoking Genetic predisposition	Tachypnea Hypoxemia Hypotension Cullen's sign Grey Turner sign	↑Amylase levels ↑Lipase levels  ↑ALT ↑ALP Leukocytosis	T-wave inversion ST-segment depression  ST-segment elevation rarely Q-waves	CT: focal or diffuse enlargement of the pancreas MRI: Pancreatic enlargement	CT Scan
	IBD	Acute, Chronic	Variable	Painful bowl movments Bloody diarrhea pus or mucus in the stool Fistula sepsis pseudo memberanous colitis	-	+	+	+	Gastric perforation Colon cancer	Genetic predisposition Alcohol abuse Smoking Microbiata and infections	Hypotension Abdominal tenderness	Electrolyte disturbance Leukocytosis	T-wave inversion ST-segment depression  ST-segment elevation rarely Q-waves	CT: Gastrointestinal inflamation	CT Scan Colonoscopy biopsy

References

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