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he intensive care unit (ICU) is the hospital facility within which the highest level of continuous
patient care and treatment care are provided.  ICU cases include a variety of severe cases
due to major surgical interventions, trauma, hemodynamic instability, sepsis and so on.  All
of these factors can easily lead to MODS (multiple organ dysfunction syndromes). 2Prof. Dr.
RS Mehta, BPKIHS
. 3. Introduction …  Multiple organ dysfunction syndromes are the leading cause of mortality
in critically ill patients and is responsible for a large amount of healthcare expenditure. 
Since the probability of death is directly correlated to the number of failing organs beyond
the kidney and the degree of physiological derangement, a clinically sensible approach is to
broaden the spectrum of physiological endpoints targeted by extracorporeal therapy. 3Prof.
Dr. RS Mehta, BPKIHS
. 4. Introduction …  Blood is the vital element that regulates all body systems from cellular to
organ level.  A multiple organ support therapy is a logical and should be the goal of
extracorporeal blood purification in the intensive care unit. 4Prof. Dr. RS Mehta, BPKIHS
. 5. Indication of ICU admission  Patients requiring, likely require, advanced respiratory
support alone.  The patient requiring support of two or more organ systems.  Patients with
co-morbidity who require support for an acute reversible failure of another organ system
5Prof. Dr. RS Mehta, BPKIHS
. 6. 6Prof. Dr. RS Mehta, BPKIHS
. 7. Clinical feature of patient requiring organ system support  Confusion  Decrease GCS 
Shortness of breath  Rapid or irregular heart beat  Rapid, shallow breathing 7Prof. Dr. RS
Mehta, BPKIHS
. 8. Clinical feature of patient requiring organ system support…  Grunting sounds  Flaring of
the nostrils  Decrease urine output= (<400ml/24 hours oliguria or 50ml/12hours anuria)
8Prof. Dr. RS Mehta, BPKIHS
. 9. Investigations  Echocardiography-two-dimensional with Doppler flow studies may show
ventricular hypertrophy, dilation of chambers, and abnormal wall motion.  ECG (resting and
exercise) may show ventricular hypertrophy and ischemia.  Chest X-ray may show
cardiomegaly, pleural effusion, and vascular congestion.  Cardiac catheterization to rule out
CAD  ABG studies may show hypoxemia due to pulmonary vascular congestion.  Liver
function studies may be altered because of hepatic congestion. 9Prof. Dr. RS Mehta, BPKIHS
. 10. Investigations…  Renal function test may be altered because of renal congestion. 
Imaging  Chest X-ray may show cardiomegaly, pleural effusion, and vascular congestion. 
Computed tomography (CT) scan is a structural imaging study that uses a computer-based X-
ray to provide a cross-sectional image of the brain.  MRI is a noninvasive structural imaging
procedure that uses powerful magnetic field and radio frequency waves to create an image of
brain and others organ.  Positron-emission tomography (PET): A computer-based functional
imaging technique that permits study of the brain's metabolism, blood flow, and chemical
processes. 10Prof. Dr. RS Mehta, BPKIHS
. 11. Objective of multiple organ support therapy  Protect the organs before organ failure 
Restrict tissue hypoxia  Reduce an excessive inflammatory response  Protect against
oxidant damage  if multiple organ failure is already established, the cells might need to be
rested. 11Prof. Dr. RS Mehta, BPKIHS
. 12. Categories of organ system support therapy  Respiratory support therapy  Circulatory
support therapy  Renal support therapy  Hemodynamic monitoring or support therapy 
Neurological monitoring or support 12Prof. Dr. RS Mehta, BPKIHS
. 13. Respiratory support therapy a. Advanced respiratory support therapy b. Basic respiratory
support therapy 13Prof. Dr. RS Mehta, BPKIHS
. 14. Advanced respiratory support  Immediate tracheal intubation and mechanical
ventilation support (excluding mask continuous positive airway pressure, CPAP) or non-
invasive ventilation. 14Prof. Dr. RS Mehta, BPKIHS
. 15. Indication  Upper and Lower airway obstruction as a result of blockage caused by blood
or pus or bronchospasm and edema.  Neuromuscular disorders as in Myasthenia gravis,
Poliomyelitis, Guillain-Barré syndrome, Snake bite and inadequate reversal of anesthesia. 
Lung diseases which prevent proper exchange of O2 and CO2 as in chest injuries
pneumothorax, lung infections, COPD, Adult Respiratory Diseases Syndrome (ARDS). 15Prof.
Dr. RS Mehta, BPKIHS
. 16. Indication …  Post-operative cardiac surgery, any other surgery, shock & trauma. 
Respiratory arrest  Acute respiratory acidosis with partial pressure of carbon dioxide (pCO2)
> 50 mmHg (normal : 35- 45) and pH < 7.25.  Hypoxemia. 16Prof. Dr. RS Mehta, BPKIHS
. 17. Basic respiratory support  Assisting in coughing, deep breathing and alveolar
recruitment techniques ( e.g., CPAP)  Chest percussion  positioning (e.g. fowlers position) 
Bronchodilators  Suctioning 17Prof. Dr. RS Mehta, BPKIHS
. 18. Basic respiratory support…  Tracheostomy care.  Physiotherapy to clear secretions at
least 2 hourly  Use of supplemental oxygen (restricted to certain situations like COPD)  Use
of an incentive spirometer to increase inhaled lung volume and eliminate mucous and saliva
18Prof. Dr. RS Mehta, BPKIHS
. 19. Basic respiratory support…  Inspiratory muscle training to help strengthen diaphragm
muscles  Nebulization  Feeding modifications to reduce aspiration risks 19Prof. Dr. RS
Mehta, BPKIHS
. 20. Indications  The possibility of progressive deterioration to the point of needing advanced
respiratory support.  Patients in whom the tracheal tube has been removed recently after
prolonged period of intubation and mechanical ventilation.  The need for mask CPAP or non-
invasive ventilation.  Patients whose trachea is intubated to protect the airway but who do
not need mechanical ventilation.  Bed ridden patients or prolonged immobility. 20Prof. Dr.
RS Mehta, BPKIHS
. 21. Nursing consideration  Assess respiratory rate and depth; Inspect thorax for symmetry of
movement.  Assess the patient for oxygenation such as oxygen saturation, signs and
symptoms of hypoxia (tachypnea, nail beds, ABG analysis, auscultation for air entry). 
Observe for tube misplacement. Prevent accidental extubation by taping tube securely,
checking q.2h.  Maintain ventilator settings as ordered.  Elevate head of bed 60-90
degrees. 21Prof. Dr. RS Mehta, BPKIHS
. 22. Circulatory support therapy  Mechanical circulatory support Use of Intra-aortic balloon
pump with a ventricular assist device (VAD).  Medical therapy including use of angiotensin
converting enzyme inhibitors, beta blockers, and aldosterone antagonists. 22Prof. Dr. RS
Mehta, BPKIHS
. 23. Intra-aortic balloon pump A ventricular assist device 23Prof. Dr. RS Mehta, BPKIHS
. 24. Indications  Cardiogenic shock resulting from acute myocardial infarction (AMI). 
Postsurgical myocardial dysfunction  Acute cardiac failure from myocarditis 
Decompensated chronic heart failure  Dilated cardiomayopathy 24Prof. Dr. RS Mehta,
BPKIHS
. 25. Nursing consideration  The nurse plays a critical role in caring for the patient receiving
intra-aortic balloon counterpulsation .  The nurse makes ongoing timing adjustments of the
balloon pump to maximize its effectiveness by synchronizing it with the cardiac cycle.  The
patient is at great risk for circulatory compromise to the leg on the side where the catheter
for the balloon has been placed; therefore, the nurse must frequently check the
neurovascular status of the lower extremities.  Auscultate heart sounds frequently and
monitor cardiac rhythm. 25Prof. Dr. RS Mehta, BPKIHS
. 26. Renal support therapy  Acute renal replacement therapy: is a term used to encompass
life- supporting treatments for renal failure. it includes: hemodialysis, peritoneal dialysis. 
Hemodialysis: Hemodialysis is a process of cleansing the blood of accumulated waste
products. In haemodialysis the blood flows through a dialysis machine that filters away the
waste products. 26Prof. Dr. RS Mehta, BPKIHS
. 27. Renal support therapy…  Peritoneal dialysis: Peritoneal dialysis involves the repeated
cycles of instilling dialysate into the peritoneal cavity , allowing time for substance exchange ,
and then removing the dialysate. PD is typically used for client with severe cardiovascular
disease 27Prof. Dr. RS Mehta, BPKIHS
. 28. Indication of dialysis  Oliguria (urine output <200 mL/12 h)  Anuria/extreme oliguria
(urine output <50 mL/12 h)  Hyperkalemia (K >6.5 mEq/L)  Severe acidemia (pH <7.1) 
Azotemia (urea >30 mg/dL)  Pulmonary edema 28Prof. Dr. RS Mehta, BPKIHS
. 29. Nursing consideration  Assess for bleeding at the access site or elsewhere. Use standard
precautions at all times. Renal failure and heparinization during dialysis increase the risk for
bleeding.  Assess for dialysis disequilibrium syndrome, with headache, nausea and vomiting,
altered level of consciousness; and hypertension.  Assess for other adverse responses to
dialysis, such as dehydration, nausea and vomiting, muscle cramps, or seizure activity. 
Assess and document vital signs, weight, and vascular access site condition.  Monitor BUN,
serum creatinine, serum electrolyte, and Hematocrit levels between dialysis treatments.
29Prof. Dr. RS Mehta, BPKIHS
. 30. Liver support therapy  Liver failure is defined as an insufficiency of any facet of liver
function to a degree that this insufficiency leads to secondary organ failures and creates a life
threatening situation if untreated.  Artificial extracorporeal liver support is a term that is
used to describe measures that are used to carry out liver function and are outside of the
body. The Molecular Adsorbent Recirculation System (MARS) is an example of artificial
extracorporeal liver support.  The ultimate goal of extracorporeal liver support is to prolong
the survival time of patients with liver failure by preventing progression of secondary organ
failure. 30Prof. Dr. RS Mehta, BPKIHS
. 31. The Molecular Adsorbent Recirculation System (MARS)  The MARS system combines the
efficacy of sorbents to remove albumin-bound toxins with the high selectivity of highly
biocompatible dialysis membranes.  In this way, common dialysis or CRRT machines can be
expanded into a modern system for liver support therapy. 31Prof. Dr. RS Mehta, BPKIHS
. 32. Nursing consideration During MARS therapy, there is potentially chance to occur
bleeding complications and mortality so observe feature of bleeding. Monitor BUN, serum
creatinine, serum electrolyte, ammonia, albumin, AST, ALT between dialysis treatments.
32Prof. Dr. RS Mehta, BPKIHS
. 33. Hemodynamic support Hemodynamics are the forces which circulate blood through the
body.  Specifically, hemodynamics is the term used to describe the intravascular pressure
and flow that occurs when the heart muscle contracts and pumps blood throughout the
body. 33Prof. Dr. RS Mehta, BPKIHS
. 34. Hemodynamic support…  Hemodynamic monitoring refers to measurement of pressure,
flow and oxygenation of blood within the cardiovascular system. Hemodynamic support
includes: Fluid resuscitation/Blood transfusion Use of vasoactive drugs like nitroglycerine,
amlodipine, nitric oxide, hydralazine. 34Prof. Dr. RS Mehta, BPKIHS
. 35. Indications  Decreased urine output from dehydration  Hemorrhage  G.I bleed  Burns
or surgery  All types of shock; cardiogenic shock, neurogenic shock or anaphylactic shock.
Any deficits or loss of cardiac function: such as myocardial infarction, congestive heart failure,
cardiomyopathy 35Prof. Dr. RS Mehta, BPKIHS
. 36. Nursing consideration  Administer fluid as prescription.  Assess the sign of cardiac
overload like dyspnea, increase CVP, edema, weight gain, crackles (rales) and bounding pulse
etc.  Measure intake and output. 36Prof. Dr. RS Mehta, BPKIHS
. 37. Neurological monitoring or support  Central venous system depression sufficient to
compromise the airway and impair protective reflexes.  Invasive neurological monitoring: 
A common complication of many serious neurologic conditions is an elevation of the pressure
within the skull, the intracranial pressure or ICP.  In adults, the average ICP ranges from <10-
15 mm Hg . 20 mm Hg is considered to be the maximal upper limit of desirable ICP and
pressures exceeding 40 mm Hg are considered extremely elevated. 37Prof. Dr. RS Mehta,
BPKIHS
. 38. Neurological monitoring or support  Whatever the underlying cause an increase in
intracranial pressure is extremely dangerous.  The type of monitor used is dependent on a
number of clinical factors, not the least of which is the neurologic disease causing the
pressure increase.  The following devices commonly used to monitor and treat intracranial
pressure: Intraventricular catheter 38Prof. Dr. RS Mehta, BPKIHS
. 39. Intraventricular catheter 39Prof. Dr. RS Mehta, BPKIHS
. 40. Nursing consideration  Proper positioning helps to reduce ICP. The head is kept in a
neutral (midline) position, maintained with the use of a cervical collar if necessary, to
promote venous drainage.  Elevation of the head is maintained at 30 degrees to aid in
venous drainage unless otherwise prescribed.  Assess the level of consciousness( GCS). 
Pupillary reaction.  Maintain aseptic technique while measuring ICP.
.
. EFINITION Peritonitis is an inflammation (irritation) of the peritoneum, the thin tissue that
lines the inner wall of the abdomen and covers most of the abdominal organs.
. 4. CAUSES AND RISK FACTOR Medical procedures, such as peritoneal dialysis. Peritoneal
dialysis uses tubes (catheters) to remove waste products from your blood when your kidneys
can no longer adequately do so. An infection may occur during peritoneal dialysis due to
unclean surroundings, poor hygiene or contaminated equipment. A ruptured appendix,
stomach ulcer or perforated colon. Any of these conditions can allow bacteria to get into the
peritoneum through a hole in your gastrointestinal tract.
. 5. CONT… Pancreatitis. Inflammation of your pancreas (pancreatitis) complicated by
infection may lead to peritonitis if the bacteria spread outside the pancreas. Diverticulitis.
Infection of small, bulging pouches in your digestive tract (diverticulitis) may cause peritonitis
if one of the pouches ruptures, spilling intestinal waste into your abdomen. Trauma. Injury
or trauma may cause peritonitis by allowing bacteria or chemicals from other parts of your
body to enter the peritoneum.Eg:accident.
. 6. SIGN AND SYMPTOM Abdomen painful Abdominal distention. Fever and chills Passing
few or no stools or gas Excessive fatigue Passing less urine Nausea and vomiting
. 7. PATHOPHYSIOLOGY Due to etiological factor Inflammation of the peritoneal cavity Abcess
of infection-due to inflammation Spread of infection throughout the body Death in severe
cases
. 8. VIDEO TIME
. 9. VIDEO
. 10. DIAGNOSTIC TEST Physical exam. Peritoneal fluid analysis.(Using a thin needle, doctor
may take a sample of the fluid in peritoneum (paracentesis) Blood tests.(TWBC) Imaging
tests (Abdominal X-ray)
. 11. TREATMENT Antibiotics are usually administered intravenously, but they may also be
infused directly into the peritoneum.Example:Ampicillin. Surgery(laparotomy) is to correct
any gross anatomical damage that may have caused peritonitis
. 12. VIDEO TIME
. 13. COMPLICATION A bloodstream infection (bacteremia). An infection throughout your
body (sepsis). Sepsis is a rapidly progressing, life-threatening condition that can cause shock
and organ failure.
. 14. PREVENTION Wash hands, including underneath fingernails and between fingers, before
touching the catheter. Clean the skin around the catheter with an antiseptic every day. Talk
with dialysis care team about proper care for peritoneal dialysis catheter.
. 15. NURSING CARE PLAN Nursing diagnosis: Deficient Fluid Volume related to Fluid shifts
from extracellular, intravascular, and interstitial compartments into intestines or peritoneal
space. Expected Outcome: Client will get enough fluid balance.
. 16. Nursing intervention with rationale: 1. Monitor vital signs, noting presence of
hypotension (including postural changes), tachycardia, tachypnea, and fever. Measure central
venous pressure (CVP) if available. Rationale: Aids in evaluating degree of fluid deficit,
effectiveness of fluid replacement therapy, and response to medications.
. 17. CON’T… 2.Observe skin and mucous membrane dryness and turgor. Note peripheral and
sacral edema. Rationale: Hypovolemia, fluid shifts, and nutritional deficits contribute to
poor skin turgor and taut edematous tissues.
. 18. CON’T… 3.Change position frequently, provide frequent skin care, and maintain dry,
wrinkle-free bedding. Rationale: Edematous tissue with compromised circulation is prone to
breakdown. 4.Maintain NPO status with NG or intestinal aspiration. Rationale: Reduces
vomiting caused by hyperactivity of bowel; manages stomach and intestinal fluids.
. 19. CON’T… 5.Measure urine specific gravity. Rationale: Reflects hydration status and
changes in renal function, which may warn of developing acute renal failure in response to
hypovolemia and effect of toxins. Note: Many antibiotics also have nephrotoxic effects that
may further affect kidney function and urine output.
.
. hock is defined as a state of cellular and tissue hypoxia due to reduced oxygen delivery
and/or increased oxygen consumption or inadequate oxygen utilization. This most commonly
occurs when there is circulatory failure manifested as hypotension (ie, reduced tissue
perfusion). Shock is initially reversible, but must be recognized and treated immediately to
prevent progression to irreversible organ dysfunction. "Undifferentiated shock" refers to the
situation where shock is recognized but the cause is unclear.
.
. CLASSIFICATION AND ETIOLOGY
. Four types of shock are recognized: distributive, cardiogenic, hypovolemic, and obstructive.
However, these are not exclusive, and many patients with circulatory failure have a
combination of more than one form of shock (multifactorial shock) (table 1). There are many
etiologies within each class, all of which are discussed in detail in the sections below. (See
'Distributive' below and 'Cardiogenic' below and 'Hypovolemic' below and 'Obstructive'
below and 'Combined' below.)
.
. Septic shock, a form of distributive shock, is the most common form of shock among patients
admitted to the intensive care unit, followed by cardiogenic and hypovolemic shock;
obstructive shock is rare [1,2]. As an example, in a trial of 1600 patients with undifferentiated
shock, septic shock occurred in 62 percent, cardiogenic shock in 16 percent, hypovolemic
shock in 16 percent, other types of distributive shock in 4 percent (eg, neurogenic shock,
anaphylaxis), and obstructive shock in 2 percent [2].
.
. In the emergency department (ED), the percentage of each type of shock seen depends upon
the population served by the ED [3,4]. As an example, busy, urban, level-I trauma centers will
see a higher percentage of hemorrhagic shock. In one study of 103 patients with
undifferentiated shock presenting to a busy, urban ED, 36 percent of patients had
hypovolemic shock, 33 percent had septic shock, 29 percent had cardiogenic, and 2 percent
had other forms of shock [3].
.
. Distributive — Distributive shock is characterized by severe peripheral vasodilatation
(vasodilatory shock). Molecules that mediate vasodilatation vary among the etiologies
discussed in the sections below.
.
. Septic shock — Sepsis, defined as a dysregulated host response to infection resulting in life-
threatening organ dysfunction [5], is the most common cause of distributive shock. Septic
shock is a subset of sepsis associated with mortality in the 40 to 50 percent range that can be
identified [6] by the use of vasopressor therapy and the presence of elevated lactate levels
(>2 mmol/L) despite adequate fluid resuscitation. The type of pathogen causing sepsis varies
with the population studied. In the United States, gram-positive bacteria (eg, Pneumococcus,
Enterococcus) are the most common pathogens responsible for severe sepsis and septic
shock. However, antibiotic-resistant organisms (eg, methicillin-resistant staphylococcus),
gram-negative organisms (eg, Pseudomonas, Klebsiella, Enterobacter), and fungi (eg,
Candida) are more commonly encountered in those with shock from sepsis, when compared
with patients who have sepsis without the features of shock. The definition, epidemiology,
prognosis, and evaluation of patients with suspected sepsis and septic shock are discussed
separately. (See "Sepsis syndromes in adults: Epidemiology, definitions, clinical presentation,
diagnosis, and prognosis" and "Evaluation and management of suspected sepsis and septic
shock in adults".)
.
. Systemic inflammatory response syndrome (SIRS) — SIRS is a clinical syndrome that is
characterized by a robust inflammatory response, usually induced by a major body insult that
can be infectious (see above) and noninfectious (list below). (See "Sepsis syndromes in
adults: Epidemiology, definitions, clinical presentation, diagnosis, and prognosis", section on
'Definitions'.)
.
. Examples of noninfectious conditions that can be complicated by SIRS include the following:
.
. ●Pancreatitis (see "Clinical manifestations and diagnosis of acute pancreatitis", section on
'Natural history and complications')
.
. ●Burns (see "Complications of severe burn injury")
.
. ●Hypoperfusion caused by trauma (see "Initial evaluation of shock in the adult trauma
patient and management of NON-hemorrhagic shock")
.
. ●Significant blunt trauma and crush injury (see "Initial evaluation of shock in the adult
trauma patient and management of NON-hemorrhagic shock")
.
. ●Amniotic fluid embolism (see "Amniotic fluid embolism")
.
. ●Air embolism (see "Air embolism")
.
. ●Fat embolism (see "Fat embolism syndrome")
.
. ●Idiopathic systemic capillary leak syndrome (see "Idiopathic systemic capillary leak
syndrome")
.
. ●Post-successful return of spontaneous circulation after a cardiac arrest [7], myocardial
infarction, or cardio-pulmonary bypass (see "Sepsis syndromes in adults: Epidemiology,
definitions, clinical presentation, diagnosis, and prognosis")
.
. Neurogenic shock — Hypotension and, in some cases, overt shock are common in patients
with severe traumatic brain injury and spinal cord injury. Interruption of autonomic
pathways, causing decreased vascular resistance and altered vagal tone, is thought to be
responsible for distributive shock in patients with spinal cord injury. However, hypovolemia
from blood loss and myocardial depression may also contribute to shock in this population.
(See "Acute traumatic spinal cord injury", section on 'Cardiovascular complications' and
"Management of acute severe traumatic brain injury", section on 'Initial evaluation and
treatment'.)
.
. Anaphylactic shock — Shock from anaphylaxis is most commonly encountered in patients
with severe, immunoglobulin-E (Ig-E) mediated, allergic reactions to insect stings, food, and
drugs. In addition to hemodynamic collapse, bronchospasm and increased airway resistance
are cardinal features of anaphylaxis. However, it can also be seen in patients with allergies to
natural rubber latex, and clinically similar but physiologically different anaphylactoid
reactions are seen in patients with allergies to iodinated contrast (table 2). (See "Anaphylaxis:
Acute diagnosis", section on 'Causes and mechanisms'.)
.
. Drug and toxin-induced shock — Drug or toxin reactions that can be associated with shock or
SIRS-like syndromes include those associated with drug overdoses (eg, long-acting narcotics);
snake bites; insect bites including scorpion envenomation and various spider bites;
transfusion reactions; heavy-metal poisoning including arsenic, iron, and thallium; and
infections associated with toxic shock syndrome (eg, Streptococcus and Escherichia spp). (See
"Use of blood products in the critically ill" and "Invasive group A streptococcal infection and
toxic shock syndrome: Epidemiology, clinical manifestations, and diagnosis".)
.
. Cyanide and carbon monoxide cause shock from mitochondrial dysfunction. (See "Cyanide
poisoning" and "Carbon monoxide poisoning" and "Inhalation injury from heat, smoke, or
chemical irritants".)
.
. Endocrine shock — Addisonian crisis (adrenal failure due to mineralocorticoid deficiency) and
myxedema can be associated with hypotension and states of shock. In states of
mineralocorticoid deficiency, vasodilatation can occur due to altered vascular tone and
aldosterone-deficiency-mediated hypovolemia. Although thyroid hormone plays a role in
blood pressure homeostasis, the exact mechanism of vasodilation in patients with myxedema
is unclear; concurrent myocardial depression or pericardial effusions likely contribute to
hypotension and shock in this population. (See "Clinical manifestations of adrenal
insufficiency in adults", section on 'Hypotension' and "Myxedema coma", section on
'Cardiovascular abnormalities' and "Cardiovascular effects of hypothyroidism".)
.
. Patients with thyrotoxicosis can develop high-output cardiac failure and do not develop shock
per se. However, with progression, these patients can develop left ventricular systolic
dysfunction and/or tachyarrhythmia, leading to hypotension. (See "Cardiovascular effects of
hyperthyroidism", section on 'Heart failure' and "Overview of the clinical manifestations of
hyperthyroidism in adults", section on 'Cardiovascular'.)
.
. Cardiogenic — Cardiogenic shock is due to intracardiac causes of cardiac pump failure that
result in reduced cardiac output (CO). Causes of cardiac pump failure are diverse, but can be
divided into the following three categories listed in the sections below (table 1).
.
. Cardiomyopathic — Cardiomyopathic causes of shock include myocardial infarction involving
greater than 40 percent of the left ventricular myocardium, myocardial infarction of any size if
accompanied by severe extensive ischemia due to multivessel coronary artery disease, severe
right ventricular infarction, acute exacerbation of heart failure in patients with severe
underlying dilated cardiomyopathy, stunned myocardium following cardiac arrest, prolonged
ischemia or cardiopulmonary bypass, myocardial depression due to advanced septic or
neurogenic shock, and myocarditis. (See "Clinical manifestations and diagnosis of cardiogenic
shock in acute myocardial infarction", section on 'Pathophysiology' and "Clinical
manifestations and diagnosis of cardiogenic shock in acute myocardial infarction", section on
'Etiology' and "Right ventricular myocardial infarction" and "Coronary artery bypass graft
surgery in patients with acute ST-elevation myocardial infarction", section on 'Cardiogenic
shock' and "Clinical manifestations and diagnosis of myocarditis in adults".)
.
. Patients with hypertrophic cardiomyopathy or severe diastolic heart failure rarely present
with cardiogenic shock, but these underlying conditions may contribute to hypotension and
shock from other causes (eg, sepsis, hypovolemia). (See "Hypertrophic cardiomyopathy:
Clinical manifestations, diagnosis, and evaluation" and "Clinical manifestations and diagnosis
of heart failure with preserved ejection fraction".)
.
. Arrhythmic — Both atrial and ventricular tachyarrhythmias and bradyarrhythmias may induce
hypotension, often contributing to states of shock. However, when CO is severely
compromised by significant rhythm disturbances (eg, sustained ventricular tachycardia,
complete heart block), patients can present with cardiogenic shock. If CO is absent because
of the underlying rhythm (eg, pulseless ventricular tachycardia, ventricular fibrillation),
patients can present in cardiac arrest. (See "Overview of atrial fibrillation" and "Wide QRS
complex tachycardias: Approach to the diagnosis" and "Ventricular arrhythmias during acute
myocardial infarction: Incidence, mechanisms, and clinical features" and "Third degree
(complete) atrioventricular block".)
.
. Mechanical — Mechanical causes of cardiogenic shock include severe aortic or mitral valve
insufficiency, and acute valvular defects due to rupture of a papillary muscle or chordae
tendineae (mitral valve defect) or retrograde dissection of the ascending aorta into the aortic
valve ring or an abscess of the aortic ring (aortic insufficiency). Additional causes include
severe ventricular septal defects or acute rupture of the intraventricular septum, atrial
myxomas, and a ruptured ventricular free wall aneurysm. While a ruptured ventricular
aneurysm can cause cardiogenic shock due to reduced output from the left ventricle, it can
also present with the features of obstructive shock, when bleeding is contained by the
pericardial sac, or catastrophic hemorrhagic shock, when the pericardial sac is breached and
hemorrhage is ongoing. (See "Acute mitral regurgitation in adults" and "Acute aortic
regurgitation in adults" and "Clinical manifestations and diagnosis of ventricular septal defect
in adults" and "Mechanical complications of acute myocardial infarction" and "Cardiac
tumors".)
.
. Critical aortic stenosis or mitral stenosis rarely present with cardiogenic shock, but often
contribute to hypotension and shock from other causes (eg, sepsis, hypovolemia). (See
"Clinical manifestations and diagnosis of aortic stenosis in adults" and "Clinical manifestations
and diagnosis of rheumatic mitral stenosis".)
.
. Hypovolemic — Hypovolemic shock is due to reduced intravascular volume (ie, reduced
preload), which, in turn, reduces CO. Hypovolemic shock can be divided into two categories:
hemorrhagic and nonhemorrhagic (table 1).
.
. Hemorrhagic — Reduced intravascular volume from blood loss can result in shock. There are
multiple causes of hemorrhagic shock, of which blunt or penetrating trauma (includes
multiple fractures without vessel injury) is the most common, followed by upper (eg, variceal
hemorrhage, peptic ulcer) or lower (eg, diverticular, arteriovenous malformation)
gastrointestinal bleeding. (See "Initial evaluation of shock in the adult trauma patient and
management of NON-hemorrhagic shock", section on 'Pathophysiology' and "Causes of
upper gastrointestinal bleeding in adults" and "Etiology of lower gastrointestinal bleeding in
adults" and "Initial management of moderate to severe hemorrhage in the adult trauma
patient", section on 'Classification of hemorrhage'.)
.
. Less common causes include intraoperative and postoperative bleeding, ruptured abdominal
aortic or left ventricle aneurysm, aortic–enteric fistula, hemorrhagic pancreatitis, iatrogenic
(eg, inadvertent biopsy of arteriovenous malformation, severed artery), tumors or abscess
erosion into major vessels, postpartum hemorrhage, uterine or vaginal hemorrhage from
other causes (eg, infection, tumors, lacerations), spontaneous peritoneal hemorrhage from
bleeding diathesis, and ruptured hematoma. (See "Management of symptomatic (non-
ruptured) and ruptured abdominal aortic aneurysm", section on 'Ruptured AAA' and "Left
ventricular aneurysm and pseudoaneurysm following acute myocardial infarction" and
"Clinical manifestations and diagnosis of acute pancreatitis" and "Overview of the
complications of peptic ulcer disease", section on 'Penetration' and "Overview of postpartum
hemorrhage" and "Managing an episode of severe or prolonged uterine bleeding", section on
'Etiology'.)
.
. Nonhemorrhagic — Reduced intravascular volume from fluid loss other than blood can cause
shock. Volume depletion from loss of sodium and water can occur from a number of
anatomic sites (see "Etiology, clinical manifestations, and diagnosis of volume depletion in
adults", section on 'Etiology'):
.
. ●Gastrointestinal losses (eg, diarrhea, vomiting, external drainage)
.
. ●Skin losses (eg, heat stroke, burns, severe dermatologic conditions including Stevens-
Johnson syndrome)
.
. ●Renal losses (eg, excessive drug-induced or osmotic diuresis, salt-wasting nephropathies,
hypoaldosteronism)
.
. ●Third space losses into the extravascular space or body cavities (eg, postoperative and
trauma, intestinal obstruction, crush injury, pancreatitis, cirrhosis)
.
. Obstructive — Obstructive shock is mostly due to extracardiac causes of cardiac pump failure
and often associated with poor right ventricle output. The causes of obstructive shock can be
divided into the following two categories, listed in the sections below (pulmonary vascular
and mechanical) (table 1).
.
. Pulmonary vascular — Most cases of obstructive shock are due to right ventricular failure
from hemodynamically significant pulmonary embolism (PE) or severe pulmonary
hypertension (PH). In these cases, the right ventricle fails because it is unable to generate
enough pressure to overcome the high pulmonary vascular resistance associated with PE or
PH. While hemodynamic collapse in the setting of PE is traditionally attributed to mechanical
obstruction, pulmonary vasoconstriction mediated by vasoactive mediators such as serotonin
and thromboxane also contribute to the observed pathophysiology [8]. Patients with severe
stenosis or with acute obstruction of the pulmonary or tricuspid valve may also fall into this
category. (See "Clinical presentation, evaluation, and diagnosis of the nonpregnant adult with
suspected acute pulmonary embolism", section on 'Hemodynamically unstable patients' and
"Clinical features and diagnosis of pulmonary hypertension of unclear etiology in adults",
section on 'Post-diagnostic testing and classification'.)
.
. Acute right heart syndrome can, given ventricular interdependence, mimic left ventricular
dysfunction resulting in cardiogenic shock. Acute right heart syndrome is associated with
myocardial infarction localizing to the right ventricle, massive volume overload, hypoxemic
vasoconstriction resulting in acute pulmonary hypertension, and pulmonary embolism. In
patients with pre-existing pulmonary hypertension and right ventricular dysfunction,
ischemia, volume overload, or hypoxemia should be avoided as these insults can result in
acute-on-chronic right ventricular dysfunction resulting in cardiovascular collapse. (See
'Cardiogenic' above.)
.
. Mechanical — Patients in this category present clinically as hypovolemic shock because their
primary physiologic disturbance is decreased preload, rather than pump failure (eg, reduced
venous return to the right atrium or inadequate right ventricle filling). Mechanical causes of
obstructive shock include the following:
.
. ●Tension pneumothorax (see "Pneumothorax in adults: Epidemiology and etiology")
.
. ●Pericardial tamponade (see "Cardiac tamponade", section on 'Physiology' and "Cardiac
tamponade", section on 'Etiology')
.
. ●Constrictive pericarditis (see "Constrictive pericarditis", section on 'Physiology' and
"Constrictive pericarditis", section on 'Etiology')
.
. ●Restrictive cardiomyopathy (see "Definition and classification of the cardiomyopathies",
section on 'Restrictive cardiomyopathy')
.
. Abdominal compartment syndrome (ACS), defined as sustained intra-abdominal
hypertension associated with organ dysfunction can exacerbate shock. Primary ACS develops
in patients with an intra-abdominal injury, whereas secondary ACS is frequently the result of
massive volume resuscitation. ACS impairs cardiovascular function by both reducing venous
return and by impairing myocardial contractility. (see "Abdominal compartment syndrome in
adults")
.
. Combined — Patients often present with combined forms of shock. Examples include:
.
. ●Patients with shock from sepsis or pancreatitis primarily have distributive shock (due to the
effects of inflammatory and anti-inflammatory cascades on vascular permeability and
peripheral vasodilation); however, they also often have a hypovolemic component (due to
decreased oral intake, insensible losses, vomiting, diarrhea) and a cardiogenic component
(due to inflammation-related myocardial depression).
.
. ●Patients with underlying cardiomyopathy may present with hypovolemic shock (from over-
diuresis) and cardiogenic shock (from inadequate compensatory tachycardia and/or stroke
volume).
.
. ●Patients with severe traumatic injury may have hemorrhagic shock from blood loss as well
as distributive shock from SIRS or, less commonly, fat embolism.
.
. ●Patients with trauma to the spinal cord can have distributive shock from injury-related
autonomic dysfunction and cardiogenic shock from myocardial depression.
.
. ●Patients with a ruptured left ventricular free wall aneurysm can have cardiogenic shock
from primary pump failure, obstructive shock from cardiac tamponade when blood loss is
contained by the pericardial sac, and hemorrhagic shock when blood loss is not contained by
the pericardial sac.
.
. ●Patients with septic shock may transition from a distributive (low systemic vascular
resistance [SVR]) shock state to multifactorial shock state after massive volume resuscitation
that results in abdominal compartment syndrome and/or acute right heart syndrome.
.
. PATHOGENESIS AND PATHOPHYSIOLOGY
. The general mechanisms, physiology, and stages of shock are discussed in the sections below
(see 'Mechanisms of shock' below and 'Physiology' below and 'Stages of shock' below). The
pathogenesis and physiology of specific forms of shock are discussed separately:
.
. ●Septic shock (see "Pathophysiology of sepsis")
.
. ●Burns (see "Burn wound infection and sepsis", section on 'Pathogenesis')
.
. ●Amniotic fluid embolism (see "Amniotic fluid embolism", section on 'Pathogenesis')
.
. ●Air embolism syndrome (see "Air embolism", section on 'Terminology and pathophysiology')
.
. ●Fat embolism syndrome (see "Fat embolism syndrome", section on 'Pathogenesis')
.
. ●Idiopathic systemic capillary leak syndrome (see "Idiopathic systemic capillary leak
syndrome", section on 'Pathogenesis')
.
. ●Spinal cord injury (see "Acute traumatic spinal cord injury", section on 'Pathophysiology')
.
. ●Anaphylactic shock (see "Pathophysiology of anaphylaxis")
.
. ●Toxic shock syndrome (see "Staphylococcal toxic shock syndrome", section on 'Microbiology
and pathogenesis')
.
. ●Myxedema coma (see "Myxedema coma", section on 'Epidemiology and risk factors' and
"Myxedema coma", section on 'Cardiovascular abnormalities')
.
. ●Cardiogenic shock (see "Pathophysiology of cardiogenic pulmonary edema")
.
. ●Pulmonary embolism (PE) (see "Overview of acute pulmonary embolism in adults", section
on 'Pathogenesis and pathophysiology')
.
. ●Pericardial tamponade (see "Cardiac tamponade", section on 'Physiology')
.
. ●Constrictive pericarditis and restrictive cardiomyopathy (see "Differentiating constrictive
pericarditis and restrictive cardiomyopathy")
.
. Mechanisms of shock — Cellular hypoxia occurs as a result of reduced tissue
perfusion/oxygen delivery and/or increased oxygen consumption or from inadequate oxygen
utilization [9-11]. Cellular hypoxia, in turn, causes cell membrane ion pump dysfunction,
intracellular edema, leakage of intracellular contents into the extracellular space, and
inadequate regulation of intracellular pH. These biochemical processes, when unchecked,
progress to the systemic level, resulting in acidosis, and endothelial dysfunction, as well as
further stimulation of inflammatory and anti-inflammatory cascades. Compounding this
process is a further reduction in tissue perfusion from complex humoral and microcirculatory
processes that impair regional blood flow [11,12].
.
. Serum lactate levels, when elevated, have traditionally been used as surrogates for
hypoperfusion and tissue hypoxia. Admittedly, lactate flux is more complex than the tissue
hypoxia hypothesis suggests, as epinephrine-mediated aerobic glycolysis in skeletal muscle
contributes to hyperlactatemia [13] as well, elevations in serum lactate level are useful risk-
stratification tools in undifferentiated shock.
.
. Physiology — The major physiologic determinants of tissue perfusion (and systemic blood
pressure [BP]) are cardiac output (CO) and systemic vascular resistance (SVR):
.
. BP = CO X SVR
. CO is the product of heart rate (HR) and stroke volume (SV):
.
. CO = HR X SV
. The stroke volume is determined by:
.
. ●Preload
.
. ●Myocardial contractility
.
. ●Afterload
.
. SVR is governed by:
.
. ●Vessel length
.
. ●Blood viscosity
.
. ●Vessel diameter (ie, vessel tone)
.
. Thus, biologic processes that change any one of these physiologic parameters can result in
hypotension and shock.
.
. The hemodynamic profiles measured on pulmonary artery catheterization that distinguish
each class of shock are shown in the tables (table 3 and table 4). Common to most forms of
shock is diminished CO and/or SVR. Occasionally, the SVR is low relative to a high CO (eg,
thyrotoxicosis), which can result in poor tissue perfusion. In general, severe hypovolemia,
cardiogenic shock, and late-stage obstructive shock are characterized by a low CO and
compensatory increase in the SVR to maintain perfusion to vital organs, whereas distributive
shock is classically associated with reduced SVR and compensatory increase in the CO.
However, the CO may be normal in the early phases of hypovolemic and obstructive shock.
Similarly, in some cases of severe distributive shock (eg, sepsis and neurogenic shock) or
combined shock, both CO and SVR may be reduced.
.
. Some forms of shock have normal CO and SVR. As an example, patients with profound
mitochondrial dysfunction (eg, inheritable mitochondrial disease, carbon monoxide, and
cyanide poisoning) are shock states that occur despite normal CO, SVR, and tissue perfusion
because they are due to inadequate oxygen utilization. (See "Mitochondrial myopathies:
Clinical features and diagnosis" and "Carbon monoxide poisoning" and "Cyanide poisoning"
and "Inhalation injury from heat, smoke, or chemical irritants".)
.
. Stages of shock — Shock is a physiologic continuum [10,14]. It begins with an inciting event,
such as a focus of infection (eg, abscess) or an injury (eg, gunshot wound), which can
progress through several stages. The early stages of shock (pre-shock, shock) are more
amenable to therapy and are more likely to be reversible, compared with end-stage shock,
which is associated with irreversible end-organ damage and death.
.
. ●Pre-shock – Pre-shock is also known as compensated shock, or cryptic shock. It is
characterized by compensatory responses to diminished tissue perfusion [15]. As an example,
in early hypovolemic pre-shock, a compensatory tachycardia and peripheral vasoconstriction
may allow an otherwise healthy adult to be asymptomatic and preserve a normal blood
pressure despite a 10 percent reduction in total effective arterial blood volume. Thus,
tachycardia, a modest change in systemic blood pressure (increase or decrease), or mild to
moderate hyperlactatemia, may be the only clinical signs of early shock [16]. Potentially, with
timely and appropriate management, deterioration can be prevented and signs of impending
deterioration can be reversed (eg, normalization of serum lactate levels).
.
. ●Shock – During shock, the compensatory mechanisms become overwhelmed, and signs and
symptoms of organ dysfunction appear including symptomatic tachycardia, dyspnea,
restlessness, diaphoresis, metabolic acidosis, hypotension, oliguria, and cool, clammy skin.
.
. The signs and symptoms of organ dysfunction typically correspond to a significant
pathophysiologic perturbation [17-19]. As examples, in hypovolemic shock, clinical signs and
symptoms are associated with a 20 to 25 percent reduction in arterial blood volume, and, in
cardiogenic shock, a fall in the cardiac index to less than 2.5 L/min/m2 is required before
signs and symptoms appear [19].
.
. ●End-organ dysfunction – Progressive shock leads to irreversible organ damage, multiorgan
failure (MOF), and death. During this stage, anuria and acute renal failure develop, acidemia
further depresses CO, hypotension becomes severe and recalcitrant to therapy,
hyperlactatemia often worsens, and restlessness evolves into obtundation and coma. Death
is common in this phase of shock.
.
. INFORMATION FOR PATIENTS
. UpToDate offers two types of patient education materials, "The Basics" and "Beyond the
Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th
grade reading level, and they answer the four or five key questions a patient might have
about a given condition. These articles are best for patients who want a general overview and
who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are
longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th
grade reading level and are best for patients who want in-depth information and are
comfortable with some medical jargon.
.
. Here are the patient education articles that are relevant to this topic. We encourage you to
print or e-mail these topics to your patients. (You can also locate patient education articles on
a variety of subjects by searching on "patient info" and the keyword(s) of interest.)
.
. ●Basics topic (see "Patient education: Shock (The Basics)")
.
. SUMMARY AND RECOMMENDATIONS
.
. ●Shock is defined as a state of cellular and tissue hypoxia due to reduced oxygen delivery
and/or increased oxygen consumption or inadequate oxygen utilization. "Undifferentiated
shock" refers to the situation where shock is recognized but the cause is unclear. (See
'Definition' above.)
.
. ●Four types of shock are recognized. However, many patients have a combination of more
than one form of shock listed below (table 1):
.
. •Distributive shock has many causes, including septic shock, systemic inflammatory response
syndrome (SIRS; eg, pancreatitis), neurogenic shock, anaphylactic shock, toxin-related shock,
and endocrine shock (eg, addisonian crisis).
.
. •Cardiogenic shock may be cardiomyopathic (eg, myocardial infarction), or due to an
arrhythmia (eg, sustained ventricular tachycardia) or a mechanical abnormality (eg, acute
valvular rupture).
.
. •Hypovolemic shock may be due to hemorrhagic (eg, trauma) or nonhemorrhagic fluid losses
(eg, vomiting).
.
. •Obstructive shock may be pulmonary vascular related (eg, pulmonary embolism [PE]) or due
to a mechanical cause of reduced preload (eg, tension pneumothorax, pericardial
tamponade).
.
. ●Cellular hypoxia results in cell membrane ion pump dysfunction, intracellular edema,
leakage of intracellular contents into the extracellular space, and inadequate regulation of
intracellular pH. These biochemical processes, in turn, progress to acidosis, endothelial
dysfunction, and further stimulation of inflammatory and anti-inflammatory cascades. (See
'Mechanisms of shock' above.)
.
. ●Common to most forms of shock is diminished cardiac output (CO) and/or systemic vascular
resistance (SVR). In general, severe hypovolemia, cardiogenic shock, and late-stage
obstructive shock are characterized by a low CO and compensatory increase in the SVR to
maintain perfusion to vital organs, whereas distributive shock is classically associated with
reduced SVR and compensatory increase in the CO. Shock due to disorders of mitochondrial
function (eg, carbon monoxide poisoning) have normal CO and SVR. (See 'Physiology' above.)
.
. ●Shock begins with an inciting event that may progress through several stages: pre-shock,
shock, and end-organ dysfunction. The progression can culminate in irreversible end-organ
damage and death. (See 'Stages of shock' above.)
.
. Use of UpToDate is subject to the Subscription and License Agreement.
. REFERENCES
. Vincent JL, De Backer D. Circulatory shock. N Engl J Med 2013; 369:1726.
. De Backer D, Biston P, Devriendt J, et al. Comparison of dopamine and norepinephrine in the
treatment of shock. N Engl J Med 2010; 362:779.
. Kheng CP, Rahman NH. The use of end-tidal carbon dioxide monitoring in patients with
hypotension in the emergency department. Int J Emerg Med 2012; 5:31.
. Jones AE, Craddock PA, Tayal VS, Kline JA. Diagnostic accuracy of left ventricular function for
identifying sepsis among emergency department patients with nontraumatic symptomatic
undifferentiated hypotension. Shock 2005; 24:513.
. Singer M, Deutschman CS, Seymour CW, et al. The Third International Consensus Definitions
for Sepsis and Septic Shock (Sepsis-3). JAMA 2016; 315:801.
. Shankar-Hari M, Phillips GS, Levy ML, et al. Developing a New Definition and Assessing New
Clinical Criteria for Septic Shock: For the Third International Consensus Definitions for Sepsis
and Septic Shock (Sepsis-3). JAMA 2016; 315:775.
. Adrie C, Laurent I, Monchi M, et al. Postresuscitation disease after cardiac arrest: a sepsis-like
syndrome? Curr Opin Crit Care 2004; 10:208.
. Smulders YM. Pathophysiology and treatment of haemodynamic
.
.
.
.
. Types of shock HYPOVOLEMIC SHOCK CARDIOGENIC SHOCK DISTRIBUTIVE SHOCK − SEPTIC
SHOCK NEUROGENIC SHOCK ANAPHYLACTIC SHOCK
. 4. Improper tissue perfusion as a result of severe loss of blood or other fluid from the body or
inadequate fluid intake , any of which decrease intravascular volume. HYPOVOLEMIC SHOCK
. 5. Causes of Hypovolemic shock Haemorragic (acute blood loss) Burns Excessive vomiting
& diarrhea
. 6. Grades of hypovolemic shock
. 7. Fluid replacement in hypovolemic shock Initiate IV therapy 6ml/kg/hr crystalloid for 1-2 hrs
---------------------------------------------------------------------------------------------------------------
Improvement No improvement Reduce IVF 3ml/kg/hr Increase IVF 10ml/kg/hr (6-12 hrs) (2
hrs) Further improvement -------------------------------------------------------------------------------
Discontinue after 24hrs Improvement No improvement Reduce to 6ml/kg/hr
----------------------------------------------- 3ml/kg/hr Hematocrit rise Haematocrit falls Discontinue
after IV Colloid Blood Transfusion 24 hrs 10 ml/kg/hr 10ml/kg/hr Improvement IVF crystalloid
Reduce to 10-6,6-3 & discontinue after 24hrs
. 8. Ionotrope : an agent that changes myocardial contractility. Vasopressor : an agent that
increases blood pressure Chronotrope : an agent that changes heart rate Dromotrope : an
agent that increases cardiac conduction velocity.
. 9. NOREPINEPHRINE Most widely used vasopressor Potent α1 agonist causing
vasoconstriction in tissue beds. Resultant increase in SVR causes rise in blood pressure.
Standard dose : 4 mg in 50 ml (0.08 mg/ml) α1 stimulation Vasoconstriction Increased SVR
Increased MAP β1 Effects  +ve chronotropic  Increases myocardial contractility
. 10. EPINEPHRINE Nature’s vasopressor Most commonly used during resuscitation cardiac
arrest and anaphylaxis. α1 : increases SVR β1 : increases HR and myocardial contractility.
β2: bronchial smooth muscle relaxation. Standard dose : 10 mg in 50 ml(0.2mg/ml)
. 11. DOPAMINE Vasopressor agent. Use in cardiogenic & septic shock. Receptor
stimulation depend on dose given Low dose :D1---------- renal perfusion Medium dose
:β1------ CO High dose : α1---------- vasoconstriction, PVR Standard dose : 0.2-1 mg/min
. 12. DOBUTAMINE A synthetic cathecholamine An inodilator β1stimulation: increase HR
and increase cardiac contractility. β2 mediated vasodilatation. Reduction in MAP is
common with dobutamine. NE usually needed to offset vasodilatation. Standard dose :
250mg in 50 ml(5mg/ml)
. 13. VASSOPRESSIN Peptide hormone released from posterior pituitary. Causes increase
permeability of DCT & CT, increases water retention.(V2 receptor) V1 receptor present in
the smooth muscle of a arteriolar wall & stimulation causes smooth muscle contraction &
vasoconstriction.
. 14. Use to augment NE action in ionotrope resistant shock. Standard dose : 60 units in 60 ml
of 0.9%NaCl ,2.4ml/hr ,fixed rate.
. 15. A state of inadequate cardiac output despite of adequate intravascular volume , resulting
in hypoxia. •Cool, mottled skin •Tachypnea •Hypotension •Altered mental status •Narrowed
pulse pressure •Rales, murmur CARDIOGENIC SHOCK
. 16. Causes of cardiogenic shock : • Acute myocardial infarction • Myocarditis • Myocardial
contusion • Aortic or mitral stenosis • Acute aortic insufficiency
. 17. Pathophysiology of cardiogenic shock:  Often after ischemia, loss of LV function  CO
reduction = lactic acidosis, hypoxia  Stroke volume is reduced  Tachycardia develops as
compensation  Ischemia and infarction worsens
. 18. Treatment of cardiogenic shock : •Aspirin, beta blocker, morphine, heparin •If no
pulmonary edema, IV fluid •If pulmonary edema •Dopamine – will ↑ HR and thus cardiac
work •Dobutamine – May drop blood pressure •Combination therapy may be more effective
•Thrombolytics(streptokinase, rt-PA) •IABP
. 19. A form of shock in which severe vasodilataion, despite normal blood volume, results in
improper distribution of blood flow.  Septic shock  Neurogenic shock  Anaphylactic shock
DISTRIBUTIVE SHOCK
. 20. Septic shock: a type of distributive shock resulting from sepsis. Sepsis : an abnormal body
wide inflammatory response to an infection that can result in death.
. 21. Pathophysiology of septic shock
. 22. Clinical signs: • Hyperthermia • Tachycardia • Wide pulse pressure • Low blood pressure
(SBP<90) • Mental status changes
. 23. Treatment of septic shock: •Fluid replacement •Supplemental oxygen •Antibiotics:
Survival correlates with how quickly the correct drug was given
. 24. Cover gram positive and gram negative bacteria-  Ceftriaxone 1 gram IV BD or 
Imipenem 1 gram IV TDS. Add additional coverage for -  Pseudomonas- Gentamicin or
Cefepime  MRSA- Vancomycin
. 25. Anaphylactic shock : develops following exposure to allergen & cross links IgE on mast
cells causing mediator release Histamine Eicosanoids-LTs,PGs Clinical presentation: Urticaria
& angioedema Bronchospasm Hyptension & CV collapse
. 26. Treatment : Epinephrine is 1st line drug Standard dose : Inj. 0.5 ml (1:1000) IM repeat
every 5-10 mins if not improve Inj. 0.5 ml (1: 10000),(1:100000) IV
. 27. Antihistaminic :  Diphenhydramine (H1), administered IV  Ranitidine (H2), administered
IV β2 agonist: salbutamol IV Corticosteroid: Hydrocortisone 200 mg IV followed by oral
prednisolone for 3 days.
. 28. Neurogenic shock : develops secondary to a sudden loss of ANS functions following spinal
cord injury resulting in vasomotor tone & impaired cellular metabolism. Features :
Hypotension Bradycardia poikilothermia
. 29. Management : Airway support. Fluid replacement. Dopamine (>10mcg/kg/min)
Ephedrine (12.5-25mg IV every 3-4 hr) Atropine
.
.
.
.
.
.
.
. Classification of Trauma
. 6. •Etiological Classification - 1. Accidental trauma. 2. Self inflicted trauma. 3.
Occupational trauma.
. 7. •Classification according to nature- 1. Physical trauma a. Perforating b.
Nonperforating c. Blunt trauma 2. Chemical trauma a. Acid b. Alkali c. Dye (Salt of acid
or alkali)
. 8. 3. Thermal trauma a. Heat b. Cold 4. Radiation trauma a. Ionizing agents b. Ultra
violet rays c. Laser burn 5. Miscellaneous
. 9. •Uniform classification based on primary evaluation; Mechanical trauma to the eye
are of two types: 1. Open globe injuries – full thickness defect of eye coats. 2. Closed
globe injuries – injuries without full thickness of eye coats.
. 10. Mechanical eye injuries Closed-globe injuries Contusion or Concussion Lamellar
laceration Superficial foreign body Open-globe injuries Laceration Rupture
Penetrating injuries Perforating injuries Intraocular FB
. 11. Assessment: •History- - should be detailed as possible - time & nature of injury -
missile,blunt,?FB remaining,chemical etc. - Past ocular history - VA, lid function -
Immunization history •Rule out life threatening injuries •Rule out globe threatening
injuries •Examine both eyes •Documentation +/- photograph •Plan for repair
. 12. Eyelid trauma
. 13. •Periocular Haematoma : - Generally innocuous but it is very important to exclude
- 1. Trauma to the globe or orbit 2. Orbital roof fracture 3. Basal skull fracture
. 14. Fig. (A) Periocular haematoma and oedema; (B) periocular haematoma and
subconjunctival haemorrhage; (C) ‘panda eyes’
. 15. •Laceration : 1. Superficial lacerations 2. Lid margin lacerations 3. Lacerations
with mild tissue loss 4. Lacerations with extensive tissue loss 5. Canalicular
lacerations
. 16. Fig. Lacerated eye injuries
. 17. Repair
. 18. •General principles of repair: 1. Clean the wound 2. Remove foreign body 3. Careful
handling of tissues 4. Careful alignment of anatomy - lid margins,lash line,skin folds,
etc. 5. Close in layers 6. Timing - Ideally within 12-24 hours of injury but can delay up
to 1 week; pt’s factors, gross swelling 7. Anaesthesia – GA / LA
. 19. Repairing procedure 1.Superficial lacerations without gaping can be sutured with
5-0 / 6-0 black silk, removed after 5 days 2.Lid margin laceration - Carefully align to
prevent notching a. Align with 5-0 silk suture b. Close tarsal plate with fine absorbable
suture (5-0 vicryl) c. Place additional marginal silk suture d. Close skin with multiple
interrupted suture 3.Lacerations with tissue loss - Primary closure and may also need
a lateral cantholysis
. 20. Fig. Repairing lid margin lacerations
. 21. 4.Canalicular lacerations repair: - Repair within 24 hours - Locate & approximate
ends - Bridge the defect with silicone tubing - Leave the tube in situ for 3-6 months
. 22. •Complications - - Lid margin notching - Lagophthalmos - Hypertrophic scar -
Infection - Tearing – canalicular damage, lid malposition, pump failure - Ptosis
. 23. Orbital fractures
. 24. Types : •Blow-out orbital floor fracture •Blow-out medial wall fracture •Roof
fracture •Lateral wall fracture
. 25. •Blow-out orbital floor fracture Cause: Sudden increase in orbital pressure by an
impacting object greater in diameter than the orbital aperture (>5 cm) e.g.- Fist, tennis
ball etc.
. 26. Mechanism of an orbital floor blow-out fracture
. 27. Signs of orbital floor blow-out fracture •Periorbital ecchymosis, oedema and
emphysema may also present •Infraorbital nerve anaesthesia •Ophthalmoplegia
tipically in up and down-gaze (double diplopia) •Enophthalmos – if severe
. 28. Investigations • Right blow-out fracture with ‘tear-drop’ sign • Restriction of right
upgaze and downgaze • Secondary overaction of left eye Coronal CT scan Hess test
. 29. Surgical repair of orbital floor blow-out fracture a. Subciliary incision • Coronal CT
scan following repair of right blow-out fracture with synthetic material b.Periosteum
elevated and entrapped orbital contents freed c.Defect repaired with
syntheticmaterial d. Periosteum sutured a b c d
. 30. Medial wall blow-out fracture Signs & Investigation • Periorbital subcutaneous
emphysema • Ophthalmoplegia - adduction and abduction if medial rectus muscle is
entrapped • CT coronal view shows fractures of the medial wall (red arrow) Treatment
• Release of entrapped tissue • Repair of bony defect
. 31. Trauma to the Globe
. 32. •Principles of Evaluation: 1.Initial assessment a. Determination of nature, extent,
life threatening problems b. History of the injury, including the circumstances, timing
and likely object c. Thorough examination of eyes and the orbits 2.Special
investigations a. Plain X-ray b. CT scan c. MRI (Never if ferrous metalic FB) d. USG (B-
scan)
. 33. Blunt Trauma
. 34. Pathogenesis of ocular damage by blunt trauma
. 35. Anterior segment complications of blunt trauma
. 36. •Corneal abrasion •Stromal oedema •Tears in Descemet membrane Corneal
complications
. 37. • Traumatic hyphaema
. 38. • Vossius ring • Radial sphincter tears • Iridodialysis Pupillary complications
. 39. • Cataract • Subluxation • Dislocation Lens complications of blunt trauma
. 40. Angle Recession Rupture globe
. 41. Posterior segment complications of blunt trauma
. 42. Commotio retinae (A) Peripheral (B) central (C) macular hole following resolution
. 43. Choroidal rupture Acute with subretinal haemorrhage Old with secondary
choroidal neovascularization
. 44. Retinal breaks and detachment Equatorial breaks Avulsion of the vitreous base
with Dialysis Macular holes
. 45. Traumatic optic neuropathy (TON) Optic nerve avulsion
. 46. Penetrating trauma
. 47. Complications of penetrating trauma Penetrating corneal wounds Flat anterior
chamber Small shelving with formed anterior chamber
. 48. Penetrating corneal wounds with lens damage with iris involvement
. 49. Anterior scleral laceration with ciliary and vitreous prolapse Scleral laceration
with iridociliary prolapse
. 50. Vitreous haemorrhage Tractional retinal detachment
. 51. Foreign body
. 52. Superficial foreign body Subtarsal foreign body Corneal foreign body with
surrounding cellular infiltration
. 53. •Management: a. Careful slit-lamp examination for exact position & depth b.
Removal under slit-lamp with 26-gause needle c. Magnetic removal for a deeply
embedded metallic foreign body c. Residual ‘rust ring’ may remove with sterile ‘burr’ d.
Antibiotic oint. with cycloplegic and/or NSAIDs
. 54. Intraocular foreign body
. 55. Intraocular foreign body (A) In the lens (B) In the angle (C) in the anterior vitreous
(D) on the retina
. 56. •Management: a. Accurate history- helpful for nature of FB b. Examination - Entry
exit point - Gonioscopy & fundoscopy must - Documentation for damaged structure c.
CT scan d. MRI contraindicated for metalic FB
. 57. Removal technique • Removal with magnet or by pars plana vitrectomy • with
forceps either through the pars plana or limbus
. 58. Chemical Injury
. 59. Key features: •Majority of injuries are accidental •Few due to assault •2/3 rd of
accidental burns occur at work place •Alkali burns are twice as common as acid
•Alkali burns more severe than acid
. 60. Grading of severity of chemical injuries Grade I (excellent prognosis) •Clear
cornea •Limbal ischaemia - nil Grade II (good prognosis) •Cornea hazy but visible iris
details •Limbal ischaemia <1/3 Grade III (guarded prognosis) •Hazy cornea with no iris
details •Limbal ischaemia 1/3 to 1/2 Grade IV (very poor prognosis) •Opaque cornea
•Limbal ischaemia >1/2 •G - II •G - III •G - IV
. 61. Medical Treatment of Chemical Injuries 1.Copious irrigation (15-30 min) – to
restore normal pH 2.Topical steroids (first 7-10 days) – to reduce inflamation 3.Topical
and systemic ascorbic acid – to enhance collagen production 4.Topical citric acid – to
inhibit neutrophil activity 5.Topical and systemic tetracycline – to inhibit collagenase
and neutrophil activity 6.Cycloplegia – to improve comfort
. 62. Surgical Management of Severe Chemical Injuries Treatment of severe corneal
opacity by keratoplasty or keratoprosthesis Division of conjunctival bands Re-
establish the fornices Correction of eyelid deformity

. Eye Trauma
. 32. Corneal injuries Corneal Abrasion  Sensation of foreign body, light sensitivity,
tearing  Local drops (Amethocaine 0.5%)  Fluorescein with blue light  Rx
Chlorsig (drops/ointment) Corneal Flash burns  Arc welding/UV lamp  Red,
painful, tearing  LA, Fluorescein  Rx Chlorsig
. 33. Corneal foreign body Dirt/glass/metal (rust ring) Velocity of impact Signs of
penetration Removal  Local  25G needle, lateral approach using slit lamp 
Dental burr for rust ring (adherent rust ring may loosen with Chlorsig/patch for 24hrs
as the cornea heals, may recall pt)
. 34. Chemical burns Acids: toilet/pool cleaner, battery fluid Alkalis (more harmful):
lime, mortar/plaster, drain cleaner, oven cleaner, ammonia Immediate Mx: LA
copious irrigation with fluid-bag of N/Saline + Morgan Lens until pH 7.5, test aquity 
Degree of vascular blanching (esp at limbus) proportional to severity of burn 
Chlorsig, Ophthal. referral
. 35. Blunt Trauma - Haemorrhage Subconjunctival Hemorrhage  usually benign, if
spont. Check BP/ Coags  If cant see post border ?Orbital # Hyphaema: blood in
anterior chamber  If >1/3 = damage to drainage angle, risk glaucoma  Mx
shield/patch/semi- recumbent/rest +/- sedation/admission no NSAIDs, Ophthal. Ref. 
Recurrent bleeding in 10% esp with early mobilization Hemorrhage vitreous or
retina, can be accompanied by a retinal detachment. Iris damage can result in poor
pupil reactivity = Traumatic mydriasis. Misleading Neuro signs  Lens can be damaged
or dislocated and a cataract may develop
. 36. Blunt trauma - Orbital blowoutfracture Usually inferior wall since weakest 
Signs:  Diplopia/Ophthalmoplegia from muscle entrapment. Tethering of inferior
rectus prohibits the upward movement of the globe.  Proptosis from swelling or
retrobulbar hemorrhage and later Enophthalmos from loss of volume  Infraorbital
nerve entrapment- numb cheek/upper teeth  Epistaxis 30% incidence of a ruptured
globe in conjunction with orbital fractures. (Wilkins RB, Havins WE. Current treatment
of blow-out fractures. Ophthalmology. May 1982;89(5):464-6)
. 37. Blowout Fracture Mx  Repair: Indicated if significant diplopia or cosmetically
unacceptable enophthalmos. Most surgeons will wait 10 to 14 days following the
trauma to allow for resolution of the associated edema and hemorrhage  Medical : if
no diplopia/enophthalmos  o antis/no nose blowing/? steroids
. 38. Ruptured Globe May be from blunt or penetrating trauma Occurs at thinnest
part:  Limbus (Visible with slit lamp)  Insertions of the extra-ocular muscles
(reduced eye movements, loss red reflex from vitreous haemorrhage)  Around the
optic nerve Signs:  Pupil : peaked, teardrop- shaped, or otherwise irregular 
Seidel’s Sign  Enophthalmos (recession of the globe within the orbit) 
Exophthalmos from retrobulbar hemorrhage
. 39. Ruptured Globe Ix: CT most sensitive Mx : Anti-
emetics/analgesics/prophylactic antibiotics/tetanus/fast  Urgent Ophthal. referral
always requires surgical intervention.  ? Suxamethonium in open globe injury
controversial, weigh up risk to airway Mx and theoretical risk of ocular extrusion and
ask opthal.
. 40. Penetrating Eye Trauma Easily missed since may seal over and abnormal signs
may be subtle High risk with high velocity eg metal striking metal and glass  Leave
bodies insitu until surgery Signs:  Distorted pupil  Cataract  Prolapsed black
uveal tissue on the ocular surface  Vitreous hemorrhage.  Seidel’s Sign 
Shallow/flat anterior chamber or bubbles in anterior chamber  Mx as for ruptured
globe
. 41. Lid Lacerations Require Ophthal. ref. if:  Torn lid margins - must be closed
accurately  Lacrimal ducts damage  Any suspicion of a foreign body or penetrating
eyelid injury  Mx refer/Tetanus/iv antis/ antiemetics/shield eye
. 42. Famous Eyes Who’s eye’s are they?
. 43. Golden Rules Always check visual acuity Always attempt to open eye early
and examine pupil/acuity etc in trauma Beware Dx unilateral conjunctivitis until
more serious disease is excluded Don’t D/C pt with LA drops - impedes healing,
further injury may occur to anaesthetized eye. Don’t start Steroid drops without
ophthalmology r/v

rue ocular emergency </li></ul><ul><li>Both acid and alkali burns can be blinding </li></ul><ul><li>-
Acid burns tend to coagulate proteins, limiting </li></ul><ul><li>the depth of penetration.
</li></ul><ul><li>- Alkali burns can rapidly penetrate the cornea, </li></ul><ul><li>causing damage to
intraocular structures. </li></ul>Chemical Ocular Injury
49. <ul><li>Immediate copious irrigation with a minimum of </li></ul><ul><li>1-2 L of saline or until
pH is normalized ( 7.3-7.7 ) </li></ul><ul><li>- Instill a topical anesthetic </li></ul><ul><li>- Use eyelid
retractor </li></ul><ul><li>- Double eversion of the eyelids </li></ul>Chemical Ocular Injury :
Management
50. Irrigation in case of chemical injury
51. <ul><li>Immediate copious irrigation with a minimum of </li></ul><ul><li>1-2 L of saline or until
pH is normalized ( 7.3-7.7 ) </li></ul><ul><li>- Instill a topical anesthetic </li></ul><ul><li>- Use eyelid
retractor </li></ul><ul><li>- Double eversion of the eyelids </li></ul>Chemical Ocular Injury :
Management <ul><li>Ophthalmologists Referral </li></ul><ul><li>No corneal involvement
</li></ul><ul><li>- ATB + steroid eye drop </li></ul>
52. Chemical Ocular Injury : Classification Grade I Grade II Grade III Grade IV
53. Chemical Ocular Injury : Management <ul><li>Preservative-free artificial tears
</li></ul><ul><li>Topical non-preserved steroid </li></ul><ul><li>Topical cycloplegic
</li></ul><ul><li>Topical antibiotics </li></ul><ul><li>Oral analgesics </li></ul><ul><li>Pressure patch
or bandage CL </li></ul><ul><li>Antiglaucoma + </li></ul>
54. Bilateral Alkali Injuries Chemical Ocular Injury
55. Chemical Ocular Injury : Management Corneal Transplantation Keratoprosthesis
56. <ul><li>Accidental into the eye can cause the lids to </li></ul><ul><li>adhere and adhesive clumps
to form on the cornea </li></ul><ul><li>Not permanently harmful to the eye
</li></ul><ul><li>Cyanoacrylates are used occasionally directly on the </li></ul><ul><li>cornea to seal
corneal perforations. </li></ul>Cyanoacrylate Glue
57. <ul><li>Moisten the glue with eye ointment, and remove </li></ul><ul><li>as much as can be
removed easily without causing </li></ul><ul><li>damage to underlying tissue </li></ul><ul><li>The
glue will loosen and become easier to remove </li></ul><ul><li>in a few days. </li></ul>Cyanoacrylate
Glue

General instructions for post operative patients after eye surgery

01. Eye shield: Please use eye shield for protection when you sleep. You may use dark glasses during daytime. Please wash
the eye shield and glasses with soap and water each day and dry the same before use.

02. Washing the face: Cleaning of the operated eye will be as per the instructions given by the doctor/ nurse. The rest of the
face can be mopped with a clean and wet cloth. Avoid splashing water into the operated eye.

03. Shaving: Shaving is permitted. But avoid splashing water after shaving. Instead, clean with a wet cloth.

04. Bathing: You can bathe below neck from the first postoperative day itself. But avoid head bath for a period of 3-4 weeks.

05. Use of facial cosmetics: Avoid cosmetics to the eye such as mascara, eye liners etc for at least 4 weeks.

06. Physical activity: Activities such as walking, talking, TV viewing can be resumed immediately after surgery. However,
Jogging, swimming, gardening, contact sports, etc may have to be avoided until 4-6 weeks after surgery.

07. Driving: Avoid driving till your surgeon gives you permission.

08. Joining back duties: Usually you will be allowed to join your duties by 4-6 weeks after surgery depending upon the
surgery. You may have to check with your doctor regards to the exact date of joining duty.

09. You may resume your sexual life a week or two after the surgery.

10. The following symptoms may be expected after most surgeries: Some amount of redness, watering, foreign body sensation,
and glare are common. The severity varies with the type of surgery. These symptoms will reduce with time and usually
disappear by 4-6 weeks.

11. If you have any worsening of the symptoms and specifically if there is increasing redness, pain or decreased vision please
report as emergency to the Sankara Nethralaya premises at 18, college Road, Nungambakkam.

Emergency Services are Available Round The Clock

12. Procedure for cleaning the eye:

A. The operated eye needs to be cleaned at least twice a day.

B. The attendant performing this task should wash the hands with soap and water and dry them with a clean towel.

C. You may use the disposable tissue supplied at the hospital for this purpose.

D. Cleaning the lower lid is done by asking the patient to look up and wiping all the secretions sticking to the lower
lid margin.

REOPERATIVE NURSING CARE OF THE PATIENT UNDERGOING OPHTHALMIC SURGERY

The eye is a delicate and important organ, and its care and protection are of the utmost importance.
Common conditions of the eye that may require surgical intervention include trauma, cataract,
glaucoma, and detached retina. The ophthalmologist will determine the treatment required and
procedure of choice in each patient's case. The procedure may vary from a simple incision to facilitate
drainage to total removal of the eyeball (enucleation).

a. Physical Orientation. The patient will require a thorough orientation to his immediate hospital
environment. This is done to help the patient during the postoperative period, since he may be blind
as a result of the procedure or the need for the eyes to be patched.

(1) Assist the patient to learn details of his room such as the location of furniture, doors, windows, and
so forth.

(2) Familiarize the patient with the voices of those who will care for him after surgery. Familiarize him
with the daily sounds and noises in the environment, since he will be more aware of sound without his
vision.

b. Observation. The patient should be observed for tendencies to cough or sneeze (smoker's cough,
allergies, and so forth). Such observations should be reported to the professional nurse for
consideration in the plan of care. Such violent movements of the head during the postoperative
course may cause increased intraocular pressure, leading to hemorrhage or rupture of incisions.

c. Education. The patient must receive a thorough education about the postoperative course of events
and his responsibilities and restrictions. The patient must understand the objective of resting the eyes
and avoiding actions that increase intraocular pressure.

(1) The head must be kept very still.


(2) No reading.

(3) No showers, no shampooing, no tub baths.

(4) No bending over at the waist.

(5) No lifting of heavy objects.

(6) No sleeping on the operative side. If both eyes are affected, the patient must sleep on his back.

d. Physical Preparation.

(1) A bowel prep is done the evening prior to surgery to prevent the patient from straining at stool
during the immediate post-op period.

(2) Shaving of eyebrows, cutting of eyelashes, and shaving of face should be done only on the order of
the surgeon.

(3) After the patient has been taken to surgery, prepare a post-op bed, ensuring that the bed is
equipped with side rails.

(4) Sand bags should be made available for use in immobilizing the head.

e. Family. Often, if the patient must be kept absolutely still or will be temporarily blinded after surgery,
a member of the family may be asked to stay with the patient. If this is the case, the family member
should receive the same orientation and education given to the patient.

. POSTOPERATIVE NURSING CARE OF THE PATIENT UNDERGOING OPHTHALMIC SURGERY

a. Return from Surgery.

(1) The patient must be lifted off the litter, he is not to move himself.

(2) The patient should be positioned in the bed as prescribed by the physician.
(3) Sandbags should be used to immobilize the patient's head, if ordered.

(4) If both eyes are bandaged (they normally are), the side rails MUST be raised at all times to protect
the patient in the event he becomes disoriented and attempts to get out of bed.

(5) Place the call bell within easy reach of the patient's head and let the patient know exactly where it
is located.

(6) Remind the patient that he should not cough, sneeze, or blow his nose. Instruct him to inform the
staff if he feels the urge, since these actions will increase intraocular pressure.

b. Orientation.

(1) Reinforce the physical orientation given during the preoperative period by verbally reviewing the
locations of objects in the room.

(2) Orient the patient to other people in the room.

(3) The patient should have an awareness of his surroundings and know what to expect to avoid being
startled or frightened.

c. Precautions.

(1) Avoid dislodgement of the eye dressings by securing them with an eye shield or reinforcing loose
tape.

(2) Restrain the arms of children and disoriented or uncooperative patients, as appropriate.

(3) A sleeping patient must be watched constantly to ensure that proper positioning is maintained.
Often, a family member may be asked to stay with the patient for this purpose.

(4) Avoid jarring or bumping the bed, as this may startle the patient.

(5) If the patient is newly blinded as a result of the surgery, observe for depression and take
precautions if patient is potentially suicidal.
(6) Check the physician's orders before giving anything by mouth. Nausea and vomiting must be
avoided. Additionally, the motion of chewing may be contraindicated.

d. Approaching the Patient. An important consideration in the care of a patient who has both eyes
bandaged is the method of approaching him.

(1) ALWAYS speak to the patient upon entering his area and before touching him.

(2) Allay the patient's fears by explaining each procedure or activity fully.

(3) Continue to reinforce his orientation to the surroundings.

(4) Always let the patient know when you are leaving his area.

e. Diversional Activity. Diversional activities will promote a relaxed atmosphere for convalescence and
prevent the patient from dwelling on his situation.

(1) Provide activities that are not fatiguing to the eyes if the eyes are not bandaged.

(a) No reading.

(b) Minimal television.

(2) Encourage visitors to chat with the patient or read to him.

(3) Encourage the use of a radio for entertainment and to keep the patient "in touch" with current
events if he is unable to read the daily newspaper.
(4)
NURSING CARE OF THE PATIENT WITH VISION LOSS

a. Physical Orientation. To prevent injury and encourage independence, the patient with vision loss
should receive a thorough orientation to his surroundings.

(1) Describe the room and its contents in detail, so that the patient can form a mental image of his
room.
(2) Lead the patient around the room, letting him feel the furniture, windows, and doorways. (3)
Orient the patient to any personnel that may be expected to enter his room. For example,
housekeeping personnel or laboratory technicians.

(4) Familiarize the patient with the sounds of his environment. Explain the source of those he is
unfamiliar with. Remember, a patient with vision loss depends heavily on his hearing for
environmental cues and orientation.

(5) Orient the patient to things around him by comparing their location to the numbers on the face of
a clock, with the patient located in the center of the clock.

(a) When describing his room, identify locations by clock reference. For example, the bathroom door is
at 2 o'clock and the door to the hallway is at 9 o'clock.

(b) When describing the food on his plate, identify the location of the food items by clock reference.
For example, the potatoes are at 12 o'clock, the green beans are at 3 o'clock, the roast beef is at 6
o'clock, and the biscuit is at 9 o'clock.

b. Precautions. To protect the patient from accidental injury, follow these guidelines.

(1) Inform the patient when something in his room has been moved or is different from usual.

(2) Keep doors completely opened or completely closed. This will prevent walking into a partially
opened door.

(3) Keep toilet articles in the location the patient places them. Do not move them without telling the
patient.

(4) Remove hazardous items such as light cords, small trash cans, and other items that the patient
could trip over.

c. Assisting the Patient.

(1) Always address the patient by name when entering his area.

(2) Always let the patient know when you are leaving his area.
(3) When walking with the patient, do not hold him or walk behind him and push him along. Allow the
patient to place his hand on your arm or shoulder and walk beside you.

(4) Encourage the patient to be independent and self-sufficient.

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