Iatrogenic

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iatrogenic

What is iatrogenic

Iatrogenic is a medical term commonly applied to illness, disorders, diseases or symptoms directly attributable to medical or surgical procedures or comments of a physician 1. The harm that a physician can do is not limited to the imprudent use of medicine or procedure, but may include unjustified remarks and misinterpretation of investigational data.

Iatrogenic causes

Here are some examples of iatrogenic causes.

Adverse effects of diagnostic procedures

Mechanical procedures

Diagnostic aspiration of fluids may lead to hemorrhage, secondary infection, etc. Rapid pleural or peritoneal fluid aspiration and needle biopsies may lead to shock and even death. Endoscopic procedure may cause perforation of hollow viscus.

Diagnostic radiology

Reactions to contrast media injected intravenously or intra-arterially may be mild, moderate or severe, and some are potentially fatal. Intravascular contrast media may have a nephrotoxic reaction. Cerebral angiography may cause transient or permanent neurological deficits. Radioisotopes are safe except in pregnant mothers or in newborn 2.

Adverse effects of therapeutic regimen

Adverse drug reactions

Adverse drug reactions is defined by World Health Organization as any response for a drug which is noxious, unintended and which occurs at doses normally used for prophylaxis, diagnosis and therapy of disease 3. Adverse drug reactions can be classified as predictable (side effects, toxicity, super infection, drug interactions) and unpredictable (intolerance, idiosyncrasy, allergy or pseudo allergy) 4.

When fewer than 6 different drugs are given in hospitalized patients, the probability of an adverse reaction is about 5%, but if more than 15 drugs are given, the probability is more than 20%. Of the patients admitted to a General hospital, 2 to 5% are due to adverse drug reactions and fatality in patients with adverse drug reactions varies from 2-12%. Adverse drug reactions occurs in the elderly more frequently 5.

To overcome the inadequacies in the WHO (World Health Organization) definition, new definition for adverse drug reaction is “an appreciably harmful or unpleasant reaction, resulting from an interaction related to the use of a medicinal product, which predicts hazard from future administration and warrants prevention or specific treatment or alteration of the dosage regimen or withdrawal of the product”. They are classified into six types (with mneminics), dose-related (Augmented), non-dose-related (Bizarre), dose-related and time-related (Chronic), time-related (Delayed), withdrawal (End of use), and failure of therapy (Failure) 6.

Anaphylaxis

Penicillin and other beta-lactum antibiotics and various types of vaccines and sera, and human insulin, are the most common agents that cause anaphylaxis. Aspirin and other nonsteroidal anti-inflammatory agents (NSAIDs) cause non-IgE mediated anaphylactoid reactions 7.

Drug induced cutaneous manifestations

Some of the cutaneous manifestations are 8:

  1. Alopaecia: Cytotoxic agents
  2. Erythema multiforme: Chlorpropamide, Sulphonamides
  3. Exanthematous eruptions: Allopurinol, Anti convulsants
  4. Exfoliative dermatitis: Gold, streptomycin
  5. Fixed drug eruptions: Barbiturates, Tetracyclines
  6. Photosensitivity: Griseofulvin, Indomethacin
  7. Toxic epidermal necrolysis: Barbiturates, Sulphonamides

Drug induced hematological disorders

Megaloblastic anemia

Oral contraceptives, phenytoin, phenobarbitone and primidone cause megaloblastic anemia due to folic acid deficiency, colchicines, neomycin, paramino salicylic acid due to vitamin B12 deficiency and 6-mercaptopurine, 5 fluro-uracil, hydroxy-urea, acyclovir and zidovudine by interfering with DNA metabolism 9.
Hemolytic anemia

Drugs causing haemolysis by direct action are phenacetin, paramino salicylic acid, sulphonamides: by immune mechanism are aminopyrine, chlorpromazine, quinine and tetracycline: and in G6PD deficient patients, antimalarials (primaquine) and antibiotics (nitrofurantoin) 10.

Aplastic anemia

Drugs that regularly produce bone marrow depression: busulphan, cyclophosphamide, chlorambucil, vinblastine, and 6 mercaptopurine. Drugs which rarely produce bone marrow depression: chloramphenicol, penicillamine, sulphonamides, isoniazid, NSAIDSs, analgin, thiouracil, anticonvulsants, anti diabetics, cimetidine, tranquilizers etc 11.

Drugs producing Neutropenia 12

  • Analgesics and NSAIDs: Indomethcin, Phenacetin, Acetaminophen, Phenyl-Butazone and Aminopyrine
  • Anticonvulsants: Phenytoin, Carbamazepine
  • Antithyroid drugs: Thiouracil, Methimazole
  • Phenothiazines: Chlorpromazine
  • Antiarrhythmic: Quinidine

Drugs that cause thrombocytopaenia 12

Alpha-methyldopa, carbimazole, chloramphenicol, cyclosporins, phenylbutazone, quinine, quinidine, rifampicin, sulphonamides etc.

Hazards of blood transfusion

Complications occur in 2 percent of blood transfusions 13.

  1. Immunological reaction: Allergic-anaphylaxis, fever, haemolysis, non cardiac pulmonary oedema.
  2. Non immunological: Circulatory overload, thrombophlebitis and embolism, bacterial contamination, transmission of diseases like malaria, hepatitis, syphilis and AIDS and transfusion siderosis in multiple transfusion.

Drug induced gastro-intestinal diseases

Oral lesions 14

  1. Lichen planus like lesions: methyldopa, chloroquine and propranolol.
  2. Lupus erythematosis like lesions: hydralazine, gold. Acid peptic disease : acetyl salicylic acid, NSAIDs, corticosteroids etc.

Pancreatitis: azathioprine, glucocorticoids and oral contraceptives.

Malabsorption: broad-spectrum antibiotics, cholestyramine and neomycin.

Hepatic damage

Drug induced liver injury is a potential complication of nearly every medication because liver metabolizes virtually all drugs. Acute (acetaminophen, halothane) and chronic (nitrofurantoin, methyldopa) hepatocellular injury, veno occlusive disease (cyclophosphamide) and hepatocellular carcinoma (sex and anabolic hormones) can all occur. There are many new drugs like glyburide, ketoconazole, lisinopril, lovastatin, ticlopidine etc. which were also associated with hepatotoxic reactions. Among causes of fulminant hepatic failure certain drugs like halothane, acetaminophen, phenytoin and alpha methyldopa account for 20-50% of cases 15.

Respiratory disorders due to drugs

Type of reaction Example of drug 14

  1. Airway obstruction (Bronchospasm): Beta-Blockers, Adenosine, NSAIDs
  2. Cough: ACE inhibitors
  3. Nasal congestion: Oral contraceptives, Reserpine, Guanithidine
  4. Pulmonary oedema: Contrast media, Methadone, Interleukin 2
  5. Pulmonary hypertension: Fenfluramine
  6. Pulmonary infiltration: Anticancer agents, Acyclovir, Amiodarone
  7. Pleural disease: Hydralazine, Methysergide
  8. Pulmonary thromboembolism: Oral contraceptives

Drug induced cardiovascular diseases

Drug reactions may lead to exacerbation of angina (alpha blockers), arrhythmias (digitals, beta-adrenergic agents, tricyclic anti-depressants and quinine), cardiomyopathy (daunorubicin, emetine and lithium), hypo or hypertension (glucocorticoids and sympathomimetics), pericardial disease (emetine, procainamide and minoxidil), and Torsades de pointes (sparfloxacin) 14.

Renal disorders caused by drugs

The kidney is the main excretory organ of the body and hence affected by most drugs 16.

  1. Directly toxic to the tubular cells: paracetamol, amphotericin B, cisplatin, sulphonamides etc.
  2. Function as an antigen or as a hapten and the resulting antigen antibody reaction damages renal interstitium and leads to acute interstitial nephritis : penicillins, cephalosporins, NSAIDs, anticoagulants, gold salts, captopril etc.
  3. Renal failure by reducing renal blood flow: noradrenaline and dopamine in high doses. NSAIDs indirectly affect renal blood flow by inhibiting production of prostaglandins.

Analgesic nephropathy – heavy and prolonged consumption of compound analgesic preparations particularly those containing phenacetin can cause chronic renal failure. This analgesic nephropathy is part of a broader analgesic syndrome, which includes hypertension, peptic ulcer, anaemia and recurrent headache.

Syndrome of drug-induced kidney disease

Common risk factors which precipitate adverse effects include old age, volume-depleted state, pre-existing renal dysfunction and co-existing use of other nephrotoxins.

Syndrome of drug-induced kidney disease

  1. Pre-renal failure/functional renal failure: NSAIDs, ACE-inhibitors, Diuretics, Interleukin-2, Amphotericin-B.
  2. Acute tubular necrosis: Aminoglycosides, Rifampicin, NSAIDs, Cyclosporine, Cisplatin
  3. Acute Interstitial nephritis: Penicillins, NSAIDs, Allopurinol, Thiazides, Sulfonamides.
  4. Thrombotic microangiopathy/hemolytic uremic syndrome: Mitomycin-C, Cyclosporine, Quinine, Cocaine, Clopidogrel.
  5. Isolated proteinuria with nephritic syndrome: Gold, heroin, Captopril, NSAIDs, IFN-alpha, D-penicillamine.
  6. Chronic tubulointerstitial disease: NSAIDs, Thiazides, Lithium, Chinese herb nephropathy, Germanium.
  7. Retroperitoneal fibrosis: Methysergide, Hydralazine, Methyldopa.

Neurological manifestations

Neurological manifestations 17

  1. Aseptic meningitis: Intravenous immunoglobulin
  2. Extra pyramidal lesions: Haloperidol, Methyl dopa, Phenothiazine
  3. Peripheral neuropathy: Isoniazid, Metronidazole, Gold salts, Nitrofurantoin, Amiodarone, Vaccines.
  4. Pseudomotor Cerebri or intracranial hypertension: Amiodarone, Glucocorticoids, Oral contraceptives
  5. Convulsions: Amphetamine, Analeptics, Lithium, Phenothiazine
  6. Stroke: Oral contraceptives
  7. Encephalitis and Guillain-Barre syndrome: Anti-rabies vaccination (purified chick embryo cell)
  8. Myopathy: Statins

Neuroleptic malignant syndrome – Rigidity, hyperthermia, altered mental status resembling catatonia, labile blood pressure and autonomic dysfunction characterize one of the serious complications of neuroleptic agents like Haloperidol 18.

Drug induced psychiatric syndromes

Drug induced psychiatric syndromes 5

  1. Delirium or Confusional state: Anticholinergics, Glucocorticoids, Phenothiazines
  2. Depression: Beta blockers, Glucocorticoids, Nifedipine
  3. Drowsiness: Antihistamines
  4. Hallucination: Beta blockers, Levodopa, Narcotics
  5. Hypomania, Mania: Glucocorticoids, Sympathomimetics
  6. Paranoid states: Amphetamines

Drug induced musculoskeletal/rheumatic disorders

Drug induced musculoskeletal/rheumatic disorders 19

  1. Arthralgia: Fluorides, growth hormone, Penicillin, Quinolones (in children), Sulphonamides
  2. Hyper-uricaemia and Gout: Cytotoxic drugs, Cyclosporine, Salicylates Ethambutol, Levodopa, Nicotinic acid, Phenytoin, Diuretics.
  3. Mylagia/Myositis: Amphotericin B, Chloroquine, Cimetidine, Clofibrate, Colchicines, Cyclosporines, Gemfibrozil, Lovastatin, Levodopa, Penicillamine, Phenytoin, Rifampicin, Vincristine, Zidovudine.
  4. Osteoporosis: Anticonvulsants, Corticosteroids, Heparin, Methotrexate.
  5. Scleroderma like disorder: Bleomycin, INH, Penicillamine, Silicon Breast implants.

Adverse reactions due to sudden stoppage of drug

Sudden stoppage of drugs can cause 20:

  1. “Rebound phenomenon” : relapse with or without exacerbation of the basic disease
  2. “Withdrawal phenomenon” : a new clinical syndrome unrelated to the original disease

Antihypertensive drugs: Sudden stoppage of clonidine and alpha methyldopa cause syndrome resembling pheochromocytoma.

Beta-blockers: Sudden stopping of the drug in coronary artery disease may cause infarction, aggravation of angina or rhythm disorders.

Corticosteroids: Withdrawal accidents are seen after prolonged treatment, unrelated to the dose and duration of treatment and relapse of basic disease even in an aggravated form.

Barbiturates: Sudden stoppage in epileptic patients can induce status epilepticus. When used to induce sleep, sudden stoppage can cause acute insomnia, confusion, agitation, hallucinations and convulsions.

Drugs producing malignant diseases

Drugs producing malignant diseases 21

  1. Leukemia (esp. acute myeloid leukemia) − Anti cancer agent, Radiotherapy, rarely Chloramphenicol and Phenyl-butazone
  2. Cancer of breast and endometrium − Estrogens, Tamoxifen
  3. Cancer of vagina − Diethyl stilbesterol
  4. Liver cancer − Anabolic steroids, Oral contraceptives

Drug nutrient interaction

Drugs may decrease nutrient absorption, increase urinary excretion, directly compete with or antagonize the nutrient from a carrier protein and interfere with the synthesis of an enzyme or coenzyme essential for the metabolism of the nutrient 22.

Drug induced fever

Drug fever constitutes one percent of all fevers of unknown origin. Any drug can cause fever (antihistamines, barbiturates, iodides, penicillins, phenytoin, propylthiouracil, β-lactum antibiotics etc). A history of allergy, skin rash or eosinophilia is often absent in cases of drug fever 23.

Adverse reactions following immunization

Adverse reactions following immunization 24

  1. Inherent vaccine induced
    • (a) Mild and common – local reaction, fever
    • (b) Moderately severe and uncommon – suppurative lymphadenitis (BCG vaccination)
    • (c) Severe and rare-Encephalopathy and hypersensitive reactions (paralytic polio following oral polio vaccine).
  2. Programmatic errors: Septic – toxic shock syndrome and abscess.

Interaction between indigenous and prescription drugs

Use of indigenous drugs is neither inquired in the drug history nor are the patients advised to avoid such an indiscriminate concurrent use of drugs. Sometimes these factors lead to either a therapeutic failure or a drug interaction or an accentuation of the unknown toxicities of the chemical prescription drugs 25.

Ophthalmological complications

Ophthalmological complications 5

  1. Cataract: Busulphan
  2. Corneal opacities: Chloroquine
  3. Colour vision alteration: Digitalis
  4. Glaucoma: Sympathomimetics
  5. Optic neuritis: Quinine
  6. Retinopathy: Chloroquine

Radiation hazards

Radiation hazards 5

  1. Acute and chronic progressive radiation injuries
  2. Pneumonitis
  3. Glomerulosclerosis and chronic interstitial nephropathy
  4. Enteritis and cystitis
  5. Venoocclusive disease of liver
  6. Bone marrow depression
  7. Malignancy

Hazards of hospitalization

The prevalence of hospital-acquired infections is around 10%. Urinary tract infections and respiratory infections are the commonest. There is increased chance of infections associated with diagnostic and therapeutic procedures and with antibiotic resistant bacterial flora 26.

Iatrogenic Cushing syndrome

Iatrogenic Cushing syndrome is Cushing syndrome due to your body being exposed to corticosteroid drugs or exogenous glucocorticoid products for a long time. Corticosteroid drugs contain a man-made version of cortisol. One example is taking oral corticosteroid medications in high doses over an extended period of time. Drugs that have been reported to result in iatrogenic Cushing syndrome are glucocorticoids, megestrol acetate, and herbal preparations that contain glucocorticoids. These medications, such as prednisone, have the same effect in the body as does cortisol produced by your body.

Oral corticosteroids may be necessary to treat inflammatory diseases, such as rheumatoid arthritis, lupus and asthma, or to prevent your body from rejecting a transplanted organ. Because the doses required to treat these conditions are often higher than the amount of cortisol your body normally needs each day, side effects from excess cortisol can occur.

It’s also possible to develop Cushing syndrome from injectable corticosteroids — for example, repeated injections for joint pain, bursitis and back pain. Inhaled steroid medicines (taken for asthma) and steroid skin creams (used for skin disorders such as eczema) are generally less likely to cause Cushing syndrome than oral corticosteroids. But, in some individuals, these medications may cause Cushing syndrome, especially if taken in high doses.

Too much cortisol can produce some of the hallmark signs of Cushing syndrome — a buffalo hump between your shoulders, a rounded face, and pink or purple stretch marks on your skin. Cushing syndrome can also result in high blood pressure, bone loss and, on occasion, type 2 diabetes.

Morbidity and mortality associated with iatrogenic Cushing syndrome are related primarily to the effects of excess glucocorticoids.

Two catastrophic medical crises that occur in glucocorticoid excess states are perforated viscera and opportunistic fungal infections. Exposure to excess glucocorticoids results in multiple medical problems, including hypertension, obesity, osteoporosis, fractures, impaired immune function, impaired wound healing, glucose intolerance, and psychosis.

Exogenous steroids suppress the hypothalamic pituitary axis, with full recovery taking as long as a year after cessation of glucocorticoid administration. Thus, patients who are on or who have taken steroids are at risk for developing an adrenal crisis if steroids are stopped or not increased during an acute illness.

Glucocorticoids’ bioavailability is between 60% and 100%. More than 90% of the circulating glucocorticoid binds to corticosteroid binding globulin. The unbound free hormone in the circulation binds to the glucocorticoid receptor (GR). Glucocorticoid receptor consists of a carboxy terminal ligand binding domain, a DNA binding domain and an N terminal domain. Except for prednisolone, which has an affinity for corticosteroid binding globulin that is about half of cortisol. Other synthetic glucocorticoids, in comparison to cortisol, have much less affinity to corticosteroid binding globulin.

Binding of the glucocorticoid to glucocorticoid receptorresults in several intracellular processes of gene transcription and translation that ultimately lead to several actions of glucocorticoids on tissues. Some glucocorticoids can have cross activity with mineralocorticoid receptor (MR) due to significant homology between glucocorticoid receptor and mineralocorticoid receptor 27.

Structural differences between glucocorticoid compounds result in different bioavailability, duration, onset of action, potency and metabolic profiles of each product. Downregulation of the nuclear factor-kappa B activation 28, changes in the enzyme adenosine monophosphate-activated protein kinase activity 29 and modulation of activator protein 1 (Fos/Jun) 30 are some of the important pathways that have been described. More research still needs to be conducted to fully understand the underlying signaling pathways and glucocorticoid tissue-specific responses.

A study by Serfling et al suggested that weight gain in iatrogenic Cushing syndrome may be related to a glucocorticoid-stimulated rise in the amygdala and insula’s blood oxygen level–dependent (BOLD) response to approach-associated food stimuli. Thus, glucocorticoids may increase the anticipated reward value of food, leading to greater food consumption 31.

Iatrogenic Cushing syndrome symptoms

Symptoms of Cushing’s syndrome can start suddenly or gradually. They tend to get slowly worse if not treated.

Common signs and symptoms of Cushing’s syndrome involve progressive obesity and skin changes, such as:

  • Weight gain and fatty tissue deposits, particularly around the midsection and upper back, in the face (moon face), and between the shoulders (buffalo hump), increased fat on your chest and tummy, but slim arms and legs
  • Pink or purple stretch marks (striae) on the skin of the abdomen, thighs, breasts and arms
  • Thinning, fragile skin that bruises easily
  • Slow healing of cuts, insect bites and infections
  • A red, puffy, rounded face
  • Acne

Cushing’s syndrome can also cause high blood pressure, which can be serious if not treated.

Women with Cushing syndrome may experience:

  • Thicker or more visible body and facial hair (hirsutism)
  • Irregular or absent menstrual periods

Men with Cushing syndrome may experience:

  • Decreased libido
  • Decreased fertility
  • Erectile dysfunction

Other signs and symptoms include:

  • Severe fatigue
  • Muscle weakness
  • Depression, anxiety and irritability
  • Loss of emotional control
  • Cognitive difficulties
  • New or worsened high blood pressure
  • Headache
  • Bone loss, leading to fractures over time
  • In children, impaired growth

Iatrogenic Cushing syndrome complications

Without treatment, complications of Cushing syndrome may include:

  • Bone loss (osteoporosis), which can result in unusual bone fractures, such as rib fractures and fractures of the bones in the feet
  • High blood pressure (hypertension)
  • Type 2 diabetes
  • Frequent or unusual infections
  • Loss of muscle mass and strength

Iatrogenic Cushing syndrome diagnosis

If you’ve been taking a corticosteroid medication for a long time, your doctor may suspect that you’ve developed Cushing syndrome as a result of this medication. If you haven’t been using a corticosteroid medication, these diagnostic tests may help pinpoint the cause:

  • Urine and blood tests. These tests measure hormone levels in your urine and blood and show whether your body is producing excessive cortisol. For the urine test, you may be asked to collect your urine over a 24-hour period. Both the urine and blood samples will be sent to a laboratory to be analyzed for cortisol levels. Your doctor might also recommend other specialized tests that evaluate the blood and urine to help determine if Cushing syndrome is present and to help identify the underlying source of any excess production. These tests often involve measuring cortisol levels before and after stimulation or suppression with other hormone medications.
  • Saliva test. Cortisol levels normally rise and fall throughout the day. In people without Cushing syndrome, levels of cortisol drop significantly in the evening. By analyzing cortisol levels from a small sample of saliva collected late at night, doctors can see if cortisol levels are too high, suggesting a diagnosis of Cushing syndrome.
  • Imaging tests. Computerized tomography scans or magnetic resonance imaging scans can provide images of your pituitary and adrenal glands to detect abnormalities, such as tumors.
  • Petrosal sinus sampling. This test can help determine whether the cause of endogenous Cushing syndrome is rooted in the pituitary or somewhere else. For the test, blood samples are taken from the petrosal sinuses — veins that drain the pituitary glands. A thin tube is inserted into your upper thigh or groin area while you’re sedated, and threaded to the petrosal sinuses. Levels of ACTH are measured from the petrosal sinuses, and from a blood sample taken from the forearm. If ACTH is higher in the sinus sample, the problem stems from the pituitary. If the ACTH levels are similar between the sinus and forearm, the root of the problem lies outside of the pituitary gland.

These tests don’t only help your doctor diagnose Cushing syndrome, they may also help rule out other medical conditions with similar signs and symptoms. For example, polycystic ovary syndrome — a hormone disorder in women with enlarged ovaries — shares some of the same signs and symptoms as Cushing has, such as excessive hair growth and irregular menstrual periods. Depression, eating disorders and alcoholism also can partially mimic Cushing syndrome.

Iatrogenic Cushing syndrome treatment

Treatments for Cushing syndrome are designed to lower the high level of cortisol in your body. The best treatment for you depends on the cause of the syndrome.

Reducing corticosteroid use. If the cause of Cushing syndrome is long-term use of corticosteroid medications, your doctor may be able to keep your Cushing signs and symptoms under control by reducing the dosage of the drug over a period of time, while still adequately managing your asthma, arthritis or other condition. For many of these medical problems, your doctor can prescribe noncorticosteroid drugs, which will allow him or her to reduce the dosage or eliminate the use of corticosteroids altogether. Don’t reduce the dose of corticosteroid drugs or stop taking them on your own. Do so only under your doctor’s supervision. Abruptly discontinuing these medications could lead to deficient cortisol levels. Slowly tapering off corticosteroid drugs allows your body to resume normal cortisol production.

Iatrogenic pneumothorax

A pneumothorax, also known as a collapsed lung, occurs when air (either from the lung or outside) collects in the space between the lung and the chest wall. Pneumothorax can present in one of three ways: spontaneous (primary), secondary, and traumatic. An iatrogenic pneumothorax is a known complication of invasive procedures such as pulmonary needle biopsy (transthoracic and transbronchial), placement of a central venous line, or positive pressure ventilation 32. However, this condition can arise from many other procedures involving the thorax and abdomen. Case reports include bilateral pneumothoraces after incorrect placement of a nebulization kit in a spontaneously breathing intubated patient 33. after insertion of a hypoglossal nerve stimulator 34, or even after acupuncture 35. Subclavian insertion of a central venous line, however, is the most common procedure associated with an iatrogenic pneumothorax 36.

In landmark-based subclavian central venous catheter placement, per Kilbourne et al. 37, six common technical errors include inadequate landmark identification, improper insertion position, insertion of the needle through periosteum, taking too shallow a trajectory with the needle, aiming the needle too cephalad, and failure to keep the needle in place for wire passage. Landmark technique also depends on the ability and experience of the medical professional performing the procedure, making iatrogenic pneumothorax more likely in a tertiary teaching hospital 38.

Iatrogenic pneumothorax is often avoidable, and in many cases can be prevented through adherence to evidence-based guidelines and procedural techniques known to reduce the incidence of iatrogenic pneumothorax 39. Ultrasound guidance during internal jugular central venous catheter insertion is associated with a lower risk as compared to guidance by anatomical landmarks 40. Other bedside procedures that are known to cause iatrogenic pneumothorax include thoracentesis. This risk can also be reduced with the use of ultrasound guidance 41.

The incidence of an iatrogenic pneumothorax is directly proportional to the number of invasive procedures performed 42. Patients in unstable trauma or code situations are more likely to undergo an invasive intervention. This along with limited access to internal jugular sites when a non-femoral vein site is desired results in an elevated risk for iatrogenic pneumothorax 43.

Iatrogenic pneumothorax signs and symptoms

The presentation in a patient with a pneumothorax can range from asymptomatic to life-threatening based on the size, rate of development, and the health of the underlying lung. An iatrogenic pneumothorax is part of a differential diagnosis in a patient with pleuritic pain and dyspnea, tachypnea, and tachycardia. Decreased or absent breath sounds on the affected side is highly suspicious. Any pneumothorax can become a tension pneumothorax. Findings could include hypoxia, hypotension, distended neck veins, a displaced trachea, and unilaterally decreased breath sounds 44.

Iatrogenic pneumothorax complications

Tension pneumothorax is the most notable complication of any pneumothorax previously described. This disorder is life-threatening and requires immediate intervention 45. Another well-described complication of pneumothorax is having a persistent air leak and/or failure of lung re-expansion, which usually require further surgical intervention 46.

Iatrogenic pneumothorax diagnosis

Iatrogenic pneumothorax can be diagnosed clinically. Point-of-care ultrasound has the advantage of being rapid, highly sensitive and specific, and easily repeatable. Suggestive findings include the lack of pleural sliding. A “point sign” (sliding pleural next to non-sliding pleura) is diagnostic. An upright posteroanterior chest radiography has 83% sensitivity 44. Chest CT is more sensitive than chest radiography but inherently results in a delay in treatment.

Iatrogenic pneumothorax treatment

First, determine if the patient is stable or unstable. Next, provide supplemental oxygen at a rate to maintain adequate oxygenation 47. Some patients with small pneumothoraces may resolve with observation 48. Definitive treatment options of a pneumothorax include needle aspiration, chest tube drainage, video-assisted thoracic surgery (VATS), and open surgical intervention 49. Treatment takes precedence over imaging. If felt to be clinically unstable, the traditional first step is to perform a needle aspiration or decompression to reduce the excess air in the pleural space. Place a large-bore needle in the second intercostal space in the midclavicular line as a temporary measure 50. Finger thoracostomy is the most recently used technique. One makes an incision over the lateral chest wall in the “safe triangle” formed by the lateral border of the pectoralis major, the lateral border of the latismus dorsi, the fifth intercostal space, and the base of the axilla. Next, one inserts a finger over the fifth intercostal space and bluntly dissects into the pleural space. It is fast and safe as it does not cause a pneumothorax and addresses the increasing girth of today’s patients. Thoracostomy is the definitive therapy and uses the negative pressure generated by a water seal or suction to reduce air in the pleural space 51. Chest tubes are inserted in either the second or third intercostal space of the midclavicular line (Monaldi position). They can also be inserted anterior to the mid-axillary line of the fourth or fifth intercostal space (Bulau position) 52. The other two treatment choices are purely surgical and reserved for severe cases 53.

Iatrogenic pneumothorax prognosis

The estimated risk of pneumothorax recurrence is 23% to 50% over a 1- to 5-year follow-up period, with the highest risk during the first month 54. However, there is no data for recurrence or incidence changes specific to iatrogenic pneumothoraces. In patients who underwent tube thoracostomy, it is safe for them to fly as early as 72 hours after tube removal without increased risk of recurrence 55.

Iatrogenic infection

Healthcare-related infections are considered a failure of the system. As much as one in 20 hospitalized patients may acquire a healthcare-related infection which may increase complications, length, and cost of the hospital stay.

Causes of hospital-acquired infections include:

  • Failure to practice basic hand hygiene.
  • Poor technique in placing indwelling Foley and vascular catheters.

Iatrogenic infection organisms

Acinetobacter baumannii has mainly been found in the intensive care unit and in other areas of the hospital where critically ill patients are managed. The bacteria do not pose a threat to healthy individuals but can lead to a severe infection in patients with a suppressed immune system. These organisms have been found to cause meningitis and pneumonia, wound infections, and urinary tract infections. Another major concern is that Acinetobacter is rapidly developing resistance to many of the commonly used antibiotics.

Bacteroides fragilis is a normal occurring organism in the colon. The organism is generally not harmful but is an opportunist. When patients take antibiotics, this cansuppress other normal flora and allow Bacteroides to enter the systemic circulation. The slow growth of bacteria and its occurrence with other colon pathogens often makes treatment difficult.

Clostridium difficile is the most well-known because of its ability to induce life-threatening colitis. The bacteria thrive in the presence of antibiotics and can easily spread via the oral-fecal route in a hospital setting. Clostridium difficile is resistant to most routine cleaning solutions, including alcohol-based sanitizers. Clostridium difficile can be treated, but in some cases, a fecal transplant may be required.

Carbapenem-resistant Enterobacteriaceae have become very common in hospitalized patients. These organisms are easily transferred from human to human by contact with skin or an infected device such as a Foley catheter. High mortality rates occur in patients who develop sepsis with these resistant organisms.

Enterococcus faecalis is a highly resistant colonic organism. Most isolated cases in hospitals reveal that this strain is resistant to vancomycin, leaving very few treatment options for patients. While enterococcus is normally found in the colon, it can enter the systemic circulation and cause sepsis, wound infections, urinary tract infections, and even pneumonia.

Escherichia coli is another gram-negative organism found in the intestinal tract, but it can become pathogenic when the opportunity arises. It is the most common cause of urinary tract infections in hospitalized patients. The 0157.H7 strain can cause hemolytic uremic syndrome.

Klebsiella pneumoniae is a common cause of pneumonia, urinary tract infections, wound infections, and meningitis. The risk of infection with Klebsiella is greater in patients with catheters and those on ventilators. Many species of Klebsiella are resistant to traditional antibiotics. These organisms are often a cause of infections in the neonatal intensive care unit and carry a high morbidity and mortality.

Other organisms that are associated with hospitalized patients include methicillin-resistant Staphylococcus aureus, Pseudomonas aeruginosa, Staphylococcus aureus, Stenotrophomonas maltophilia, and vancomycin-resistant Staphylococcus aureus.

Iatrogenic infection prevention

Appropriate hand-washing is one of the single most effective methods to decrease infection transfer. High-risk procedures such as indwelling Foley catheter and vascular catheter infection rates can be decreased by adhering to the use of sepsis bundles.

Effective hand washing is linked to decreased morbidity and mortality rates. Sink availability or alcohol-based hand rubs prevent nosocomial infections. The Centers for Disease Control and Prevention guidelines include:

  • Avoiding artificial nails.
  • Changing gloves after each patient is evaluated or treated.
  • Keeping natural nails less than one-fourth of an inch long.
  • Use alcohol-based hand rubs.
  • Washing hands with soap and water.

Hospital-acquired pneumonia causes significant morbidity and mortality. Risk factors include anemia, malnutrition, chronic renal failure, depressed mental status, thoracic surgery, and recent hospitalization. While decreasing hospital-acquired infections is a difficulty, attention to risk factors and interventions may help decrease the incidence. Clostridium difficile-associated infection has become a significant problem. Clostridium difficile is most associated with the use of clindamycin, cephalosporin, and penicillin and warrants frequent surveillance.

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