Open access peer-reviewed chapter

Life Threatening but Preventable and Treatable Medical Complications of Abdominal Trauma

Written By

Raghavi Abhilesh Bembey and Ram Babu

Submitted: 10 June 2022 Reviewed: 27 June 2022 Published: 29 March 2023

DOI: 10.5772/intechopen.106134

From the Edited Volume

Abdominal Trauma - New Solutions to Old Problems

Edited by Dmitry Victorovich Garbuzenko

Chapter metrics overview

62 Chapter Downloads

View Full Metrics

Abstract

Management of the patient who underwent trauma involves simultaneous interaction buy different physicians and surgeons. The physician, surgeon and anesthesiologist usually form a team, all of whom bring their different perspective and expertise for treatment of the patient. This starts a series of events that culminates in medical evaluation, anesthetic assessment, preoperative assessment, perioperative management and post operative management of the patient as a whole. The evaluation of any trauma patient begins with evaluating the airway, accessing the breathing, and managing the circulation. After deep initial management of the patient either surgical or medical, prognosis of patient depends on follow up monitoring and care, as mortality in such patients is very high due to complications as listed below, whose early diagnosis and management will be discussed in detail in our chapter: inadequate resuscitation; delays in diagnosis and treatment; intra-abdominal sepsis; deep vein thrombosis, pulmonary embolism and thromboembolic events; hematological disorders like anemias, bleeding disorders, thrombocytopenia etc.; cardiac complications like arrhythmias, stress cardiomyopathy etc.; pulmonary and gastrointestinal complications like HAP, paralytic ileus, GERD etc.; metabolic disorders like acidosis, alkalosis, dyselectrolemia etc.; trauma complicated due to pregnancy, addictions and comorbid conditions like DM, HTN etc.

Keywords

  • abdominal trauma
  • sepsis
  • thromboembolisim
  • arrhythmias
  • acute dialysis
  • post traumatic jaundice
  • hyperkalemia

1. Introduction

Abdominal trauma causes multi system disorder with many reasons causing morbidity and mortality. While the primary site of injury is given utmost importance, simultaneous initial resuscitation should be initiated at the earliest. Here in this chapter we try and discuss very common, lethal complications of abdominal trauma which are commonly missed leading to bad outcome. A multidisciplinary team is needed to treat the patient as a whole and therefore need multiple referrals and consultation.

After initial evaluation and management as following a detailed survey needs to be done:-.

  • Primary survey: A, B, C, D, E evaluation and stabilization of Airway, Breathing, Circulation, Disability (neurologic status), and Exposure/Environmental control.

  • Secondary survey: Head-to-toe examination after initial stabilization.

  • Selective use of CT and other imaging studies.

Evaluation and treatment are done simultaneously. Done as A, B, C, D, E, for Airway, Breathing, Circulation, Disability (neurologic status), and Exposure/Environmental control. All major body systems are thoroughly and rapidly examined for any serious injury or abnormalities (known as primary survey); followed by a very detailed examination (known as secondary survey), once the patient is stabilized.

The 10 Commandments for powerful consultation have been pro-posed by using Goldman and associates in 1983 [1]. 1. To determine the question and address the question. 2. To perform the consultation in a timely. 3. To perform a thorough evaluation. 4. Writing a concise and appropriate consultation report. 5. Recommendations needed should be made clear and concise. 6. To provide early and prompt communication. 7. Do not “clear for OR.” Physician should identify all risks and attempt to correct them and optimize the patient for surgery. 8. To provide detailed, routinely and appropriate follow-up. 9. Role should be known appropriately: pure consultant versus co-manager. 10. Provide treatment options and alternative approaches and teach others tactfully.

Advertisement

2. Preoperative assessment of patient

Regular test needed for every patient needs haemogram, liver and function test, urinalysis, sugars, electrocardiography and chest X ray.

Advertisement

3. Antimicrobial prophylaxis

Factors involved in the development of postoperative infections [2] (Table 1):

  • Pathogenic bacteria present at operative site in significant numbers.

  • Environment of local wound: tissue fluids, blood, necrotic tissue

  • Host immune status: age, immunocopromised, diabetes mellitus, obesity and nutrition

  • Surgical skills needed and length of procedure.

  • Presence of foreign body.

  • Type of surgical procedure.

3.1 Non-antimicrobial interventions to decrease surgical site and related infections

  • Preoperatively

    • reduce preoperative hospitalization.

    • Treatment of remote sites of infection prior to surgery.

    • Clipping of hair at site preferred, avoid shaving or delay until time of surgery.

    • Appropriate use of antibiotics preoperatively.

    • Correction of malnutrition and deficiencies.

    • Strict diabetes control.

  • Intraoperatively/postoperatively

    • Skin preparation done carefully.

    • Rigorous use of aseptic technique.

    • High-flow filtered air or laminar flow use.

    • Reducing dead space.

    • Minimize the use of and duration of catheters and intravenous lines postoperatively.

    • Adequate hydration, oxygenation, and nutrition needs to be maintained postoperatively

3.2 General principles of antibiotic selection and use

See Table 2.

Type of procedureDefinition
CleanAtraumatic; with no break; gastrointestinal, respiratory, genitourinary tracts not entered
Clean contaminatedRespiratory or gastrointestinal tract are entered but no spillage; entry into oropharynx, sterile genitourinary, or biliary tract; minor break in technique
ContaminatedAcute inflammation present; urine or bile infected; gross spillage
from gastrointestinal tract
DirtyEstablished infection

Table 1.

Classification of surgical procedures by degree of contamination and risk of subsequent infection [3].

Nature of operationCommon pathogensRecommended drugsAdult dose before surger#
Cardiothoracic (including pacemaker placement)Staphylococcus aureus, Staphylococcus epidermidisCefazolin
Cefuroxime
Vancomycin
1–2 g IV
1.5 g IV
1 g IV
Gastrointestinal
Esophageal, gastroduodenalEnteric gram negative
bacilli, gram-
positive cocci
Cefazolin1–2 g IV
Biliary tract
(including cholecystectomy)
Enteric gram-negative
Bacilli, enterococci, clostridia
Cefazolin1–2 g IV
Colorectal (including appendectomy, non-perforated)Enteric gram-negative
bacilli, anaerobes,
enterococci
Oral: neomycin
plus erythromycin base OR
metronidazole
Parenteral: ertapenem or cefotetan or cefoxitin OR
cefazolin plus
metronidazole$
1 g IV
1–2 g IV
1–2 g IV
1–2 g IV
0.5–1 g IV
Rupture of viscusAnaerobes, Enteric gram-negative
bacilli,
enterococci
Ertapenem or
cefoxitin or
cefotetan with or without gentamicin$
1 g IV
1–2 g IV
1–2 g IV
1.5 mg/kg IV q8h
GenitourinaryEnterococci, enteric gram-negative
bacilli
Ciprofloxacin500 mg PO or 400 mg IV
Gynecologic and
Obstetric trauma
Enteric gram-negative
bacilli, anaerobes,
group B streptococci, enterococci
Cefotetan or
cefoxitin or
cefazolin
1–2 g IV
1–2 g IV
1–2 g IV
Abortion and Dilatation and curettageEnteric gram-negative
bacilli, anaerobes,
group B streptococci, enterococci
First trimester:-
Aqueous penicillin G OR doxycycline
Second trimester:
Cefazolin
2 million units IV
300 mg PO
1–2 g IV
Vascular
Arterial surgery involving a pros-
thesis, abdominal aorta, or
groin incision
S. aureus,
S. epidermidis, enteric gram-negative bacilli
Cefazolin OR
Vancomycin
1–2 g IV
1 g IV

Table 2.

Antimicrobial prophylaxis for prevention of specific surgical site infections [4].

Given as single dose within 60 min before operation. For prolonged operations, additional doses may be necessary. If vancomycin or a fluoroquinolone is used, give 60 to 120 min before incision.


Continue for 3 to 5 days post trauma. Need to expand coverage for nosocomial pathogens in postoperative dehiscence.


3.3 Causes of post traumatic and surgical fever

  • Non-infectious

    Adrenal insufficiency

    Alcohol withdrawal

    Atelectasis

    Blood (hematoma/CSF)

    Dehydration

    Drug fever (including anesthetics)

    Intravascular device infections

    Malignant hyperthermia

    Myocardial infarction

    Neoplasms, rhabdomyolysis

    Pancreatitis

    Pheochromocytoma

    Pericarditis/Dressler’s syndrome

    Pulmonary embolism

    Thyrotoxicosis

    Tissue trauma

    Transfusion reaction

  • Infectious causes

    Abscess

    Bloodstream infections

    Cholecystitis

    Clostridium difficile colitis

    Endocarditis

    Infusion-related infections

    Parotitis, Peritonitis

    Pneumonia

    Prostatitis

    Surgical site infections

    Superficial incisional infection

    Deep incisional/space infection

    Thrombophlebitis

    Transfusion related(CMV, hepatitis)

    Urinary tract infection

Advertisement

4. Patients AT high risk for regurgitation of gastric contents

Regurgitation of gastric contents needs to be prevented in trauma patient at it leads to multiple complications like aspiration pneumonia, ARDS, metabolic disturbances etc.

  • Gastric Distention

    • preoperative fasting is inadequate

      1. gastric emptying delayed

      2. Functional

      3. Obesity

      4. Pain

      5. Sepsis

      6. Uremia

      7. Pregnancy

      8. Shock

      9. Stupor/coma

      10. Autonomic neuropathy (e.g., diabetes, Shy-Drager syndrome)

      11. Recent abdominal surgery

    • Drug-induced

      1. Anticholinergics

      2. Opioids

      3. Antiparkinsonian agents

    • Intestinal obstruction/pseudo-obstruction

      1. Alcohol ingestion

  • Gastroesophageal Reflux:- drug induced, idiopathic, obesity or pregnancy related, collagen-vascular diseases

  • Esophageal Disease like neoplasms, foreign body, webs or strictures

Advertisement

5. Risk factors for venous thromboembolism

  • Surgery

  • Trauma (major or lower extremity)

  • Advanced age

  • Obesity

  • Central venous catheters

  • Heart or respiratory failure

  • Immobility, paresis

  • Previous deep vein thrombosis or pulmonary embolism

  • Varicose veins

  • Inflammatory bowel disease

  • Pregnancy and the postpartum period

  • Estrogen-containing oral contraceptives or hormone replacement therapy, Selective estrogen-receptor modulators

  • Myeloproliferative disorders, Paroxysmal nocturnal hemoglobinuria

  • Smoking

  • Malignant disease

  • Cancer therapy (hormonal therapy, chemotherapy, or radiotherapy)

  • Nephrotic syndrome

  • Inherited or acquired thrombophilia

5.1 Prophylaxis for thromboembolisim

  • Heparin prophylaxis

    • 5000 U subcutaneously administered 2 h before surgery.

    • 5000 U subcutaneously administered, q8h or q12h postoperatively.

This regimen is followed until the patient is discharged.

  • Low-molecular-weight heparin prophlaxis

    Dalteparin: 5000 U subcutaneously administered, q24h (to be initiated on evening of surgery).

    Fondaparinux: 2.5 mg, subcutaneously administered, started 6 h after surgery followed by once daily.

    Enoxaparin: 40 mg subcutaneously administered, q24 hourly (to be initiated on evening of surgery). 30 mg administered subcutaneously q24h, if creatinine clearance of less than 30 mL/min [5].

  • WARFARIN PROPHYLAXIS

  1. 10 mg by mouth the evening before surgery.

    5 mg by mouth the evening of surgery

    Adjust dose daily based on an INR of 2 to 3.

    Maintain warfarin until discharge.

  2. 10 mg by mouth the evening of surgery.

    No warfarin on postoperative day 1

    On postoperative day 2, begin warfarin to adjust INR to 2 to 3

    Maintain warfarin until discharge

We recommend the following regimen for prophylaxis post surgery for abdominal trauma:-

  • Low-risk surgery including minor procedure, no risk factors for VTE, age > 40 years:- ambulation initiated at the earliest postoperatively.

  • Moderate-risk surgery including non major procedure, age >60 years with no VTE risk factors, age 40–60 years with VTE risk factors or major procedure.

    Treatment:- Heparin: 5000 U, SC, q12 hourly.

    Enoxaparin: 40 mg, SC, started 12 h postoperatively, followed by 40 mg, SC, q24 hourly.

    Dalteparin: 5000 IU, SC, started 12 h postoperatively, followed by 5000 IU, SC, q24 hourly

  • High-risk surgery including non major surgery with age > 60 yr.; VTE risk factors; major surgery, age > 40 yr., or presence of VTE risk factors

    Treatment:-Heparin: 5000 U q8 hourly.

    Enoxaparin: 40 mg, SC, started 12 hourly postoperatively, followed by 40 mg, SC, q24 hourly.

    Dalteparin: 2500 IU, SC, 1–2 h preoperatively then 2500 IU, SC, 12 h postoperatively, followed by 5000 IU, SC, q24 hourly

  • Very high-risk surgery including major surgery, multiple VTE risk factors present or age >60 years

    Treatment: External pneumatic compression with anticoagulant therapy including;- Heparin: 5000 U, SC, q8 hourly.

    Enoxaparin: 40 mg, SC, started 12 hours postoperatively, then 40 mg, SC, q24 hourly.

    Dalteparin: 5000 IU, SC, started 12 h postoperatively, followed by 5000 IU, SC, q24 hourly [6].

Advertisement

6. Evaluation of heamatological disorders

Internal bleeding is a major complication of both blunt and penetrating trauma. Signs and symptoms are Abdominal pain, distension of abdomen and these symptoms get worse as the bleeding continues. Light-headedness, fainting can cause hypotension and hypovolemic shock. A large area of skin can get deep purple stained known as ecchymosis caused as a result from bleeding into the skin or soft tissues [7] (Figures 1 and 2).

Figure 1.

Diagnostic evaluation of anemia. MCV, mean corpuscular.

Figure 2.

Evaluation of erythrocytosis.

6.1 Indications for phlebotomy in erythrocytosis

  • Relative erythrocytosis: Not indicated.

  • Stress erythrocytosis: Not indicated.

  • Appropriate erythrocytosis resulting from cardiopulmonary disease: To hematocrit 50–60%.

  • Inappropriate primary erythrocytosis (polycythemia vera): To hematocrit <45%.

  • Inappropriate secondary erythrocytosis: To hematocrit <50%.

Other common hematological disorders needing attention:- sickle cell anemia, leukcopenia, nutritional deficiencies, bone marrow suppression, thalassemia, chronic renal failure, hemolytic anemias etc.

Figure 3.

Coagulation scheme with anticoagulant mechanisms. FSP:- fibrin split products; PT:-prothrombin time; PTT:- partial thromboplastin time; tPA:- tissue plasminogen activator.

6.2 Steps of homeostasis

Injury to vessel wall ➔ primary vasoconstriction ➔ interaction of von Willebrand protein with sub endothelium ➔ formation of platelet plug ➔ fibrin formation ➔ clot dissolution and endothelial regeneration (Figure 3).

Assessment of homeostasis: careful history, bleeding time, prothrombin time, APTT, PT-INR, platelet count (Table 3).

PathophysiologyCausesSignificant findings
Production decreasedAplastic anemialeukopenia, anemia, abnormal bone marrow, Folate deficiency abnormal, vitamin B12 low, radiotherapy or chemotherapy
SequestrationhypersplenisimSplenomegaly, hypercellular bone marrow, anemia, leukopenia, normal smear
Destruction increasedIdiopathic thrombocytopenic
purpura, acquired immunodeficiency
syndrome, drug induced, systemic
lupus erythematosus
Hematocrit,white blood cell count are usually normal with
normal smear, megakaryocytic hyperplasia

Table 3.

Causes of thrombocytopenia: which needed to be treated according to cause after abdominal trauma for optimal homeostasis.

Differential diagnosis for deranged coagulation test

  • Prolonged bleeding time: Thrombocytopenia, von Willebrand disease, platelet function defect,

  • Prolonged PT: liver disease, vitamin K deficiency, factor VII deficiency, warfarin use

  • Prolonged PTT: Factor XII, XI, IX, or VIII deficiency, von Willebrand disease, heparin induced, DIC.

  • Prolonged PT and PTT: Vitamin K deficiency, DIC, warfarin induced.

After diagnosis of bleeding disorder the treatment should be initiated accordingly with platelet or fresh frozen plasma infusions, corticosteroids, anti D etc [8].

Advertisement

7. Assessment of respiratory pathologies

See Figures 4 and 5.

Figure 4.

Pathophysiology of the events leading to postoperative pulmonary complications. V/Q, ventilation/perfusion.

Figure 5.

Pathogenesis of major post traumatic pulmonary complications.

7.1 Risk factors for post traumatic pulmonary complications

See Table 4.

Patient-relatedProcedure-related
  • General health and nutritional status

    Age

    Low albumin

  • >Functional status

    Weight loss >10%

    ASA Class

    Goldman class

  • Respiratory status

    COPD history

    Tobacco use

    Sputum production

    Pneumonia

    Dyspnea

    OSA

  • Neurological status

    Impaired sensorium

  • CVA history

  • Fluid status

  • CHF history

  • Renal failure

    Low or high BUN

  • Preoperative blood transfusion

  • Immune status

  • Chronic steroid use

  • Alcohol use

  • Incision near diaphragm

    Thoracic surgery

    Upper abdominal surgery

    AAA repair

  • Surgery technique

    Open vs. laparoscopic

  • Anesthesia duration >2 h

  • Use of spinal/epidural anesthesia vs. general anesthesia

  • Use of long-acting neuromuscular blockade (pancuronium)

  • Pain control with parenteral narcotics vs. epidural analgesia

  • Postoperative Nasogastric tube placement

Table 4.

Risk factors for post traumatic pulmonary complication.

7.2 Causes of post traumatic pleural effusions

A) Transudate:-

  • Congestive heart failure

  • Hypervolemia

  • Ascites

  • Misplaced central venous catheter

  • Pulmonary embolism (rarely)

  • Postpericardiotomy syndrome

  • Diaphragmatic contusion

B) Exudate:-

  • Pneumonia

  • Pulmonary embolism

  • Subphrenic abscess

  • Empyema

  • Atelectasis

Advertisement

8. Assessment of cardiovascular diseaes

8.1 Clinical predictors of increased perioperative cardiovascular risk (myocardial infarction, congestive heart failure, death)

  • Major [9]

    • Unstable coronary syndromes

    • Acute MI (documented MI less than 7 days previously)

    • Recent (greater than 7 days but less than or equal to 30 days).

    • Significant arrhythmias

    • myocardial infarction with evidence of important ischemic risk by clinical symptoms or non-invasive study

    • Severe valvular disease

    • Unstable or severe angina (Canadian class III or IV)

    • High grade atrioventricular block

    • Symptomatic ventricular arrhythmias in the presence of underlying heart disease

    • Decompensated congestive heart failure

    • Supraventricular arrhythmias with uncontrolled ventricular rate

  • Intermediate

    • Previous myocardial infarction by history or pathologic Q waves

    • Mild angina pectoris (Canadian class I or II)

    • congestive heart failure

    • Renal insufficiency (serum Cr > 2.0 mg/dl)

    • Diabetes mellitus

  • Minor

    • Abnormal electrocardiogram (left ventricular hypertrophy, left bundle branch block, ST–T abnormalities)

    • Low functional capacity like inability to climb one flight of stairs

    • Rhythm other than sinus (e.g., atrial fibrillation)

    • Advanced age

    • History of cerebrovascular accident

    • Uncontrolled systemic hypertension

8.2 Arrhythmias and conduction abnormalities

  • Perioperative risk factors for arrythmia:

    • male sex

    • age 70 years or older

    • significant valvular disease

    • history of supraventricular arrhythmia, asthma, congestive heart failure

    • premature atrial complexes on preoperative electrocardiography

  • Common arrhythmias in abdominal trauma patients

    • Sinus tachycardia:- Sinus tachycardia is a rhythm abnormality, usually benign. Heart rate is between 100 and 160 beats/min, regular rhythm with a normal P wave before each QRS complex.

    • Reflex bradycardia.

    • Atrial premature contractions, atrial flutter and fibrillation.

    • Paroxysmal supraventricular tachycardia:- characterized by the sudden onset of a rapid regular rhythm with rates between 150 and 250 beats/min.

    • Multifocal atrial tachycardia (MAT):- is an automatic arrhythmia characterized by an atrial rate greater than 100 beats/min with organized, discrete, non-sinus P-waves with at least three different forms in the same electrocardiographic lead.

    • Ventricular premature contractions and non-sustained ventricular tachycardia.

    • Sustained ventricular tachycardia and ventricular Fibrillation.

    • Long QT syndrome:- is a heterogeneous group of disorders characterized by a prolonged QT interval when corrected for heart rate, malignant ventricular arrhythmias (classically the torsades de pointes form of ventricular tachycardia), and the risk of sudden death. Causes:- Antiarrhythmic drugs (Type IA agents (e.g., quinidine), Type III agents (Amiodarone), Tricyclic antidepressants, antibiotics (e.g., erythromycin, azithromycin, ketoconazole), Metabolic and electrolyte disorders (Hypokalemia, Hypomagnesemia), Nutritional disorders (starvation, liquid protein diets), Subarachnoid hemorrhage, Intracerebral hemorrhage, Head trauma, Encephalitis.

8.3 Indications for implantation of cardiac pacemakers

  • Third-degree or advanced second-degree AV block associated with symptomatic bradycardia [10]

  • Second-degree AV block with symptomatic bradycardia, bifascicular block with intermittent complete heart block with symptomatic bradycardia or symptomatic bifascicular block with intermittent type II block

  • Second-degree AV block with sinus node dysfunction and symptomatic bradycardia

  • After acute myocardial infarction with persistent second-degree AV block, bilateral bundle–branch block or third-degree AV block.

  • Symptomatic and persistent second- or third-degree AV block.

8.4 Endocarditis prophylactic regimens for gastrointestinal injury surgery in abdominal trauma patient

Bacterial endocarditis prophylaxis is indicated for patients with specific cardiac structural abnormalities who are at risk for bacteremia resulting from the disruption of mucosal surfaces colonized with bacteria [11] (Table 5).

SituationAgentRegimen
High-risk patientsAmpicillin and gentamicinAdults: ampicillin 2gms intravenous or intramuscular and gentamicin 1.5 mg/kg
(maximum dose 120 mg) 1st dose administered within 30 mints of initiation of
Procedure followed 6 h later, ampicillin 1 g intravenous or intramuscular or oral amoxicillin
1 gms.
Children: ampicillin 50 mg/kg intravenous or intramuscular (maximum dose 2gms)
and gentamicin 1.5 mg/kg, 1st dose administered within 30 mints of initiation of
procedure followed 6 h later with ampicillin 25 mg/kg intramuscular r intravenous or oral
amoxicillin 25 mg/kg
High-risk patients with allergy to penicillin groupVancomycin and gentamicinAdults: vancomycin 1gm intravenous over 1–2 h with gentamicin
1.5 mg/kg, intravenous or intramuscular (maximum dose 120 mg),
injection/infusion completed within 30 min of initiation of surgery
Children: vancomycin 20 mg/kg, intravenous over 1–2 h with
gentamicin 1.5 mg/kg, intravenous or intramuscular, injection/
infusion completed within 30 min of initiation of surgery
Moderate risk patientAmoxicillin/ ampicillinAdults: Oral amoxicillin 2gms, 1 h before sugery, or
ampicillin 2gms intravenous or intramuscular, to be given with 30 min of initiation of surgery
Children: Oral amoxicillin 50 mg/kg, given 1 h before surgery,
or ampicillin 50 mg/kg intravenous or intramuscular, within 30 min of initiation of surgery
Moderate-risk with allergy
to penicillin group
vancomycinAdults: vancomycin 1gm, intravenous, infused over 1–2 h,
within 30 min of surgery initiation
Children: vancomycin 20 mg/kg, intravenous, infusion completed over 1–2 h of 30 min of surgery initiation.

Table 5.

Antibiotic prophylaxis for prevention of bacterial endocarditis in trauma patients.

Advertisement

9. Assessment of gastrontestinal diseases

9.1 Factors that contribute to prolonged postoperative ileus

  • Underlying medical conditions

    • Sepsis

    • Collagen vascular diseases

    • Amyloidosis

    • Diabetes mellitus

    • Thyroid disease

    • Peritonitis

    • Ischemic bowel disease

    • Electrolyte disturbances (e.g., hypokalemia)

  • Intraoperative bowel manipulation

    • Open surgical procedure

    • Type of anesthesia

  • Drugs

    • Opiates (e.g., morphine, codeine)

    • Opioids (e.g., fentanyl, pethidine, tramadol)

    • Nonsteroidal anti-inflammatory drugs (e.g., diclofenac, naproxen)

    • Phenytoin

    • Anticholinergic agents (e.g., trihexyphenidyl, benztropine, amantadine)

9.2 Factors that contribute to colonic PSEUDO-obstruction

  • Age

  • Alcoholism

  • Drugs

    • Narcotics

    • Antidepressants

    • Anticholinergics

    • Clonidine

    • Phenothiazines

  • Metabolic causes

  • Electrolyte imbalance

  • Acid–base disturbances

  • Hypothyroidism

  • Diabetes mellitus

  • Uremia

  • Sepsis

  • Inflammatory processes (e.g., pancreatitis and cholecy stitis)

  • Infection

  • Respiratory failure

9.3 Factors contributing to post- trauma nausea, vomiting

  • Length of anesthesia

  • Type of trauma (abdominal, gynecologic, urologic etc)

  • Female

  • Drugs

    • General anesthetics

    • Opiate analgesics

    • Digitalis

  • Postoperative ileus or pain

  • Gastroparesis

  • Refeeding after prolonged disuse of gastrointestinal tract

  • Inflammatory processes

    • Peritonitis

    • Acute pancreatitis or cholecystitis

  • Metabolic factors

    • Uremia

    • Hyperglycemia/hypoglycemia

  • Electrolyte disturbances

  • Dehydration

  • Mechanical causes

    • Gastric outlet obstruction

    • Intestinal obstruction

Other complications which are common post trauma are gastrointestinal bleeding, gastric and stress ulcers, diarrhea, esophagitis, ischaemic collitis, pseudomembrane collitis, Mesenteric Ischemia and Infarction, Colonic Diverticulosis and angiodysplasia, intra abdominal hemorrhage [12].

9.4 Causes of post traumatic jaundice

See Table 6.

Increased hepatic bilirubin loadIntrahepatic parenchymal disease
Hemolysis after Transfusions
  • Haematoma

  • Underlying hemolytic anemia

  • Drugs

    • Antibiotics

    • Amoxicillin-clavulanic acid

    • Penicillins

    • Rifampin

    • Chloramphenicol

    • Sulfonamides

    • Erythromycins

    • Tetracycline

    • Isoniazid

    • Nitrofurantoin

    • Anesthetic drugs

Pre existing liver disease
Gilbert’s syndrome(Unconjugated hyperbilirubinemia resulting from a congenital defect in the
hepatic uptake of bilirubi)
Dubin-Johnson syndrome(Conjugated hyperbilirubinemia resulting from a congenital defect in secretion
of bilirubin from hepatocytes)
  • Other drugs

  • Androgens, estrogens

  • Phenothiazines

  • Phenytoin

  • Fluconazole

  • Methyldopa

Extrahepatic Obstruction
  • Common bile duct stone

  • Cholecystitis

  • Pancreatitis

  • Biliary stricture, leak, or tumor

  • Other Causes

Parenteral nutrition
Viral hepatitis
Sepsis
Ischemic hepatitis

Table 6.

Post traumatic jaundice causes.

9.5 Local complications of abdominal trauma

Early Late

Wound infection Ulcer recurrence

Anastomotic leak Recurrent bleeding from ulcer

Bile duct injury Gastric outlet obstruction

Delayed gastric emptying Afferent loop syndrome

Anastomotic bleeding Dumping syndrome

Anemia Malabsorption

Bile reflux gastritis

Postvagotomy diarrhea

Osteomalacia and osteoporosis

Post-gastrectomy carcinoma

Pancreatitis

Advertisement

10. Assessment of renal disoders, electrolyte imbalance

10.1 Causes of perioperative renal failure

  • Decreased renal perfusion

    • Intravascular volume depletion

    • Congestive heart failure

    • Sepsis

    • Cardiopulmonary bypass

    • Anesthetic effects on renal blood flow

    • Aortic cross-clamping

    • Use of non-steroidal anti-inflammatory drugs or cycloxygenase inhibitors

    • Use of angiotensin converting enzyme inhibitors/angiotensin receptor blockers

  • Nephrotoxin exposure

    • Aminoglycosides

    • Radiocontrast agents

    • Anesthetic agents

    • Myoglobin/rhabdomyolysis

10.2 Indications for acute dialysis

  • Symptoms and signs associated with uremia in patients with creatinine clearance <20–25 ml/min per 1.73 m2 [13].

  • Nausea, vomiting, anorexia.

  • Other gastrointestinal symptoms (gastritis with hemorrhage, colitis with or without hemorrhage).

  • Altered mental status (lethargy, somnolence, malaise, stupor, coma, or delirium).

  • Signs of uremic encephalopathy (asterixis, multifocal clonus, or seizures).

  • Pericariditis.

  • Bleeding diathesis from uremic platelet dysfunction.

  • Refractory or progressive fluid overload.

  • Uncontrolled hyperkalemia.

  • Severe metabolic acidosis, especially in an oliguric patient.

  • Acute and progressive worsening of renal function with.

  • Blood urea nitrogen levels >70–100 mg/dl.

  • Measured creatinine clearance <15–20 ml/min.

10.3 Causes of peritraumatic hyperkalemia

Hyperkalemia is very commonly associated with trauma reason of which are enlisted below (Table 7).

MechanisimCauses
Increased potassium load
  • Increased catabolism

  • Blood transfusion

  • Reabsorption of hematoma

  • Tissue breakdown

  • Red blood cell salvage

  • Potassium administration

Impaired transcellular
potassium shift
  • Fasting state (insulinopenia)

  • Beta blockers

Decreased potassium
excretion
  • Volume depletion

  • Constipation

  • Medications:-Trimethoprim-sulfamethoxazole, Potassium sparing diuretics, Angiotensin converting enzyme inhibitors, Angiotensin receptor blockers

Table 7.

Hyperkalemia in trauma patient—causes.

11. Assessment of other disorders and abdominal injury

11.1 Management of adrenal insufficiency

  • Inquire about any preoperative use of glucocorticoids (systemic or inhaled) and symptoms suggestive of adrenal insufficiency.

  • Administer hydrocortisone 100 mg intravenously q 8 h. Give first dose at least 1 h before induction of anesthesia.

  • Once the patient is stable after operation, taper the hydrocortisone dose over 3–4 days to maintenance levels (30 mg/d in at least two divided doses) or to the patient’s preoperative dose of glucocorticoid.

  • Prevent volume depletion and hypoglycemia with the use of intravenous saline and glucose.

11.2 Approach to the delirious postoperative patient

  • Detection is key; maintain high index of suspicion, especially for quiet, hypoactive delirious states. Consider bedside tests of memory and orientation or administration of more formal instruments such as Confusion Assessment Method (CAM).

  • Review all medications, including those that the patient may have been taking prior to hospitalization. Remember that several common medications have significant anticholinergic effects.

  • Focused physical examination to detect infection, comorbid conditions causing hypoxia and pain due to injury. Assess volume status and rule out fecal impaction and urinary retention. Neurological examination to detect new, focal deficits.

  • Further laboratory evaluation, as clinically appropriate may include complete blood count, serum electrolytes, pulse oximetry/arterial blood gas analysis and urinalysis. Consider chest X-ray to rule out pneumonia.

  • Management strategies include environmental modifications, supportive measures and pharmacological treatment [14].

Risk factor for developing delirium in trauma patient:

  • Age

  • Preexisting central nervous system disease (e.g., dementia, Parkinson disease)

  • Type and duration of surgery

  • Sensory impairment (e.g., visual and hearing deficits)

  • Hypoxia

  • Metabolic derangements (e.g., hyponatremia, hyperglycemia, acid–base disorders, etc.)

  • Infections

  • Uncontrolled pain

  • Chronic alcoholism

  • Benzodiazepine dependence

11.3 Delayed consequences of abdominal trauma

  • Rupture of hematoma

  • Intra-abdominal abscess

  • Obstruction or ileus of bowel

  • Biliary leakage and/or biloma

  • Abdominal compartment syndrome

  • Delayed incisional hernia

    • Hematomas usually resolve spontaneously over time, depending on the size and location. Splenic hematomas or hepatic hematomas may rupture, causing significant delayed hemorrhage. Intestinal wall hematomas may perforate, typically within 48 to 72 h after injury, releasing intestinal contents and causing peritonitis, but without causing significant hemorrhage. Intestinal wall hematoma can cause intestinal stricture, typically months to years later.

    • Intra-abdominal abscess is the result of undetected hollow viscus perforation but may be a complication of laparotomy.

    • Bowel obstruction may develop after injury due to intestinal wall hematoma or adhesions caused by intestinal serosal or mesenteric tears. More commonly bowel obstruction is a complication of exploratory laparotomy.

    • Liver injury or bile duct injury can be lead to biliary leakage or biloma. Biliary leakage cause a systemic inflammatory response, severe pain or hyperbilirubinemia.

    • Abdominal compartment syndrome is similar to extremity compartment syndrome. Mesenteric and intestinal capillary leakage caused by prolonged abdominal surgical procedures, shock, systemic inflammatory response syndrome [SIRS] or systemic ischemia–reperfusion injury causing abdominal tissue edema. Peritoneal edema and ascites, increases intra-abdominal pressure (that is pressure more than 20 mm Hg), leading to pain, dysfunction of organs due to ischemia. A vicious cycle is formed where intestinal ischemia further causes edema .

    • Other affected organs dysfunction including renal insufficiency, elevated abdominal pressure interfering with respiration further causing hypoxemia or hypercarbia, decreased venous return from the lower extremities leading to hypotension, intracranial pressure increases due to increased central venous pressure, inadequate venous drainage from brain, decreased cerebral perfusion, worsening intracranial injuries.

Abdominal compartment syndrome occurs when there is vascular leak and high-volume fluid resuscitation usually more than 10 l. Develops after severe abdominal injury accompanied by shock, severe burns, sepsis, and pancreatitis also.

11.4 Spleenic injury

See Table 8.

GradesInjury
1Subcapsular hematoma involving less than 10% of surface area or laceration less than1 cm.
2Subcapsular hematoma involving 10–50% of surface area, intraparenchymal hematoma less than 5 cm n size or laceration 1–3 cm deep sparing the trabecular vessel
3Subcapsular hematoma involving more than 50% of surface area, intraparenchymal hematoma more than or equal to 5 cm in size, ruptured or expanding hematoma or laceration more than 3 cm deep or involvement of a trabecular vessel
4Laceration involving segmental or hilar vessels which devascularizes more than 25% of spleen
5Completely shattered spleen
Hilar vascular injury that devascularizes spleen

Table 8.

Grade of splenic injury.

The diagnosis is made with CT scan, followed by observation, angio-embolization, surgical repair or splenectomy.

11.5 Hepatic injury

See Table 9.

GradeInjury
1Subcapsular hematoma involving less than 10% of surface or laceration less than 1 cm.
2Subcapsular hematoma involving 10–50% of surface area, intra-parenchymal hematoma less than 10 cm in size or laceration 1–3 cm deep and less than 10 cm in size
3Subcapsular hematoma involving more than 50% of surface area, intra-parenchymal hematoma more than 10 cm size or ruptured or expanding hematoma or laceration more than 3 cm deep
4Parenchymal disruption involving 25–75% of a hepatic lobe or 1–3 Couinaud segments within a single lobe
5Parenchymal disruption involving more than 75% of one hepatic lobe or more than 3 Couinaud segments or juxtahepatic venous injuries present involving retrohepatic vena cava or central major hepatic veins
6Hepatic avulsion

Table 9.

Grades of hepatic injury.

Diagnosis confirmed with CT scan followed by observation and surgical intervention [15].

11.6 Renal injury

  • Renal injuries can be classified into severity of following 5 grades:

    • Grade 1: Subcapsular hematoma with or without renal contusion.

    • Grade 2: Laceration less than or equal to 1 cm in depth without any urinary extravasation.

    • Grade 3: Laceration more than 1 cm without urinary extravasation.

    • Grade 4: Laceration which involve collecting system with extravasation of urine; renal vascular injury of any segment; renal infarction; renal pelvis laceration with or without disruption of ureteropelvic.

    • Grade 5: Shattering or devascularization of kidney with active bleeding; main renal vascular avulsion or laceration.

  • High-grade renal injury (significant deceleration injury, direct blow to flanks) is suspected if after blunt trauma any of the following occur;

    • Gross hematuria.

    • Microscopic hematuria with hypotension (systolic pressure < 90 mmHg).

    • Diffuse abdominal tenderness.

    • Vertebral transverse process or rib fractures [15].

  • Diagnosis confirmed with clinical evaluation, CT scan, urinalysis. Treatment involves strict bed rest with close monitoring of vitals, surgical repair, angiographic intervention.

11.7 Urogenital organs

Bladder, testicular, urethral and uretral injury are common with abdominal trauma, need to be confirmed with ultrasonography, retrograde urethrography and CT scan, followed by surgical intervention and correction.

12. Discussion

The abdomen is one of the most common organs to be injured in any form of trauma. The initial resuscitation, primary and second survey, followed by FAST (focused assessment with sonography in trauma) can detect injuries. During follow up treatment detailed blood investigatins, ultasonography, CT scan of abdomen and others can detect injury of liver, spleen, pancreas, bowel alongwith common complications like intra abdominal bleeding, perforations, peritonitis etc. which can be managed surgically with laparotomy or non surgically. Also common medical conditions like uncontrolled sugars, blood pressures, rheumatological, asthma and other chronic disorders are very paticularly considered and corrected by the team of treating physicians. However, this chapter discusses the complications which very commonly occur in post trauma patients but are missed,as the main focus of treatment is limited around the trauma injury itself. In regular planned surgeries proper and stringent pre operative check up is done, optimization of patient is done, followed with srict antiseptic technique, but in trauma patient where time is the key to save the patients life these actions are often missed with lack of time to optimize the patient medically for a surgery. Sepis commonly occurs in trauma patients mostly due to primary contamination of the trauma site, but also laxity in following of antiseptic conditions, which can easily be avoided by antibiotic prophylaxis, interventions to reduce surgical site infetions as mentioned, classification of the wound, early recognition of post operative causes of fever and treatment intiation accordingly. In abdominal trauma,patient’s fasting status is not known and measures to prevent gastic content aspiration should be taken which may otherwise later lead to aspiration pneumonia, sepsis, etc. These patients are usually on bed rest for prolonged periods post trauma increasing the risk of venous thromboembolic events like pulmonary embolisim, strokes etc., which can be prevented with early mobilization, physiotherapy and adequate anticoagulation therapy. The dilemma of producing bleeds in trauma patients with anticoagulations can very well be avoided with strict monitoring and proper dosing as discussed in the chapter. Intra abdominal bleeds and hemorrhagic shock are diagnosed and treated with blood transfusions, intravenous fluids, vasopressors as and when needed, but other hematological complications like anemia, platelet disorders, coagulation disorder, erythrocytosis need attention and treatment. Assessment and attaining homeostasis helps in early recovery of wound and patient. Post traumatic lung complications are mentioned which need to be addressed as mentioned,as they can lead to prolonged need of ventilatory support and delayed healing. Cardiac abnormalities like arrhythmias and endocarditis are common in trauma patient and can lead to mortality. Acute renal injury due to pre renal and renal causes with elctrolyte imbalances can lead to early and fast deterioration of patient. Delirium in post traumatic patients is not uncommon and had multiple reasons, most of which if diagnosed timely can be treated completely, preventing any psychological sequelae. We attempt to discuss and bring into light the missed complications of abdominal trauma, so as to keep these in mind during treating an abdominal trauma patient, as the eyes see what the mind knows. The conditions mentioned above can easily be treated, significantly reducing mortality and morbidity, giving good quality of life to patient post recovery. However, treatment for each of these is beyond the scope of the chapter.

13. Conclusion

Abdominal trauma is the third organ system affected in trauma [16]. It is either blunt abdominal or penetrating abdominal trauma. While there are multiple modalities to diagnose with FAST, and other hidden trauma along with common complications. The chapter tries to cover the rare and very commonly missed complications of abdominal trauma, which are of utmost importance and can be easily diagnosed. We discuss complications like sepsis, gastric content regurgitation, ileus and obstruction, venous thrombo-embolisim, bleeding causing hemorrhagic shock, hematological complications, cardiovascular disorders like arrhythmias, endocarditis, renal and electrolyte disorders, dehydration, delirium, solid organ injuries. These in particular are addressed as these are ignored and lead to late mortality even after primary stabilization and hemodynamic correction. Timely treatment of these conditions leads to a good prognosis, significantly reducing morbidity and mortality associated with missed diagnosis of above mentioned complications. Thus, at the end we would like to conclude that treating a trauma patient as a whole is more important than just the injury.

References

  1. 1. Goldman L, Lee T, Rudd P. Ten commandments for effective consultation. Archives of Internal Medicine. 1983;143:1753-1755
  2. 2. Classen DC, Evans RS, Pestotnik SL, et al. The timing of prophylactic administration of antibiotics and the risk of surgical wound infection. The New England Journal of Medicine. 1992;326:281-286
  3. 3. Bratzler DW, Houck PM. For the surgical infection prevention guideline writers workgroup: Antimicrobial prophylaxis for surgery: An advisory statement from the National Surgical Infection Prevention Project. Clinical Infectious Diseases. 2004;38:1706-1715
  4. 4. Bratzler DW, Houck PM, Richards C, et al. Use of antimicrobial prophylaxis for major surgery: Baseline results from the national surgical infection prevention project. Archives of Surgery. 2005;140:174-182
  5. 5. Clagett G, Reisch J. Prevention of venous thromboembolism in general surgical patients: Results of meta-analysis. Annals of Surgery. 1988;208:227-239
  6. 6. Nicolaides A, Fareed J, Kakkar A, et al. Prevention and treatment of venous thromboembolism: International consensus statement (guidelines according to scientific evidence). International Angiology. 2006;25:101-161
  7. 7. Holcomb JB, Tilley BC, Baraniuk S, et al. Transfusion of plasma, platelets, and red blood cells in a 1:1:1 vs a 1:1:2 ratio and mortality in patients with severe trauma. JAMA. 2015;313(5):471-482. DOI: 10.1001/jama.2015.12
  8. 8. Armas-Loughran B, Kalra R, Carson JL. Evaluation and management of anemia and bleeding disorders in surgical patients. The Medical Clinics of North America. 2003;87:229-242
  9. 9. Compare L. Grading of angina pectoris. Circulation. 1976;54:522-523
  10. 10. Groh W, Silka MJ, Oliver RP, Halperin D, McAnulty JH, Kron J. Use of implantable cardioverter—Defibrillator in the congenital long QT syndrome. The American Journal of Cardiology. 1996;78:703-706
  11. 11. Dajani A, Taubert K, Wilson W, et al. Prevention of bacterial endocarditis. Circulation. 1997;96:358
  12. 12. Apfel CC, Korttila K, Abdalla M, et al. A factorial trial of six interventions for the prevention of postoperative nausea and vomiting. The New England Journal of Medicine. 2004;350:2441-2451
  13. 13. Chertow GM, Lazarus JM, Paganini EP, et al. Predictors of mortality and the provision of dialysis in patients with acute tubular necrosis. Journal of American Society of Nephrology. 1998;9:692-698
  14. 14. Rummans TA, Evans JM, Krahn LE, et al. Delirium in elderly patients: Evaluation and management. Mayo Clinic Proceedings. 1995;70:989-O998
  15. 15. Stassen NA, Bhullar I, Cheng JD. Nonoperative management of blunt hepatic injury: An Eastern Association for the Surgery of Trauma practice management guideline. Journal of Trauma and Acute Care Surgery. 2012;73:S288-S293. DOI: 10.1097/TA.0b013e318270160d
  16. 16. Haagsma JA, Graetz N, Bolliger I, Naghavi M, Higashi H, Mullany EC, et al. The global burden of injury: Incidence, mortality, disability-adjusted life years and time trends from the global burden of disease study 2013. International Journal of Prevention. 2016;22(1):3-18. DOI: 10.1136/injuryprev-2015-041616. Epub 2015 Dec 3. PMID: 26635210, PMCID: PMC4752630

Written By

Raghavi Abhilesh Bembey and Ram Babu

Submitted: 10 June 2022 Reviewed: 27 June 2022 Published: 29 March 2023