MEDICAL SURGICAL NURSING Best
MEDICAL SURGICAL NURSING Best
MEDICAL SURGICAL NURSING Best
MEDICAL SURGICAL
NURSING
MAIN OBJECTIVE:
To acquire knowledge on medical-surgical nursing and develop skills
and attitudes in the management of patients with medical and
surgical conditions.
SUB-OBJECTIVES
The student will be able to:
1. Discuss historical development of Medicine and Surgery.
2. Classify the disease/condition according to their etiology.
3. Describe the disease process (Pathophysiology)
4. Describe common medical-surgical conditions
Assignment
• The patient/client: the one with health care needs. Care should
be focused on the patient /client. Identification of the immediate
health care need is a fundamental nursing requirement
PROCESS OF INFLAMMATION
Introduction
INFLAMMATION:
VASCULAR EVENTS/RESPONSE
a) Hemodynamic changes
b) Altered vascular permeability
CELLULAR EVENTS/RESPONSE
c) Exudation of leukocytes
d) Phagocytosis
VASCULAR EVENTS/RESPONSE
a) Hemodynamic changes
• Dietary factors,
• Physical activity,
• Smoking
• Obesity
• Alcohol consumption
• Stress can affect inflammation.
DISORDERS OF INFLAMMATION
Inflammatory abnormalities are a large group of disorders that
underlie a vast variety of human diseases.
DIET: Provide easily digestible diet (light diet), keep the fluid
balance, and give high protein diet for the formation of new tissue
to build up the destroyed tissue.
SEDATION: Inflammation will produce pain, therefore sedative
drugs may be given to induce sleep.
The type of surgery will depend on the type of internal abscess and
where it is in the body.
Prevention of abscesses
Causes:
• A carbuncle usually develops when Staphylococcus aureus
bacteria enter the hair follicles.
Entrance/Portal site:
• insect bite and broken skin make it easy for bacteria to enter the
body and cause an infection.
• This can result in boils or carbuncles (a cluster of boils) filled with
fluid and pus.
Location:
• Carbuncles are common on the back of the neck, shoulders, or
thigh. They can also appear on the face, armpits, or buttocks
• Preventions:
• Wash your hands regularly with soap. Or use an alcohol-based hand
rub often. Careful hand-washing is your best defense against germs.
• Keep wounds covered. Keep cuts and abrasions clean and covered with
sterile, dry bandages until they heal.
• Avoid sharing personal items. Don't share towels, sheets, razors, clothing,
athletic equipment and other personal items
Comparison: carbuncle & furuncle.
Furuncle Carbuncle
• Begins as a painful infection of a single hair • It involves a group of infected hair
follicle. follicles in one skin location.
• Also known as cluster of boils.
• Also known as boil • Is a deeper skin infection
• Not as deep as carbuncles. • Carbuncles affect the deeper layers, and
• Furuncles, affect a hair follicle and they can lead to scarring.
surrounding tissue. • Carbuncle infections tend to be deeper
and more severe
• This infection is not so deep. • They take longer to develop and to
resolve than furuncles. (often leave a
• Furuncles may go away without any scar)
intervention. May burst and heal without a
scar within 2 days to 3 weeks.
CELLULITIS
CELLULITIS
• Inflammation of subcutaneous tissues as a result of bacterial
infection on any part of the body but mostly on lower limbs
Causative organisms
Streptococcus, staphylococus and H. influenzae after gaining
entry through bites, breaks in the skin.
Risk factors:
• Administer IV if:
1. Systemic signs of toxicity (eg, fever >38°C, hypotension, or
sustained tachycardia)
2. Rapid progression of erythema
3. Progression of clinical findings after 48 hours of oral antibiotic
therapy
4. Inability to tolerate oral therapy
5. Proximity of the lesion to an indwelling medical device (ex:
prosthetic joint)
Medical treatment for non-purulent cellulitis
Orals medications:
1.Clindamycin
2.Amoxicillin PLUS septrin
3.Amoxicillin PLUS doxycycline
4.Amoxicillin PLUS minocycline
Intravenous meds
5.Vancomycin
6.Oxacillin
Medical treatment for purulent cellulitis and Skin Abscesses
Orals medications:
Clindamycin, septrin, doxycycline, minocycline
Intravenous meds
Vancomycin PLUS one of the following:
1.Ampicillin
2.Ceftriaxone + metronidazole
3.Ciprofloxacin + metronidazole
4.Levofloxacin + metronidazole
• PO options after s/s resolution:
• clindamycin, SEPTRIN, or tetracyclines (doxycycline or
minocycline)
• Duration of treatment:
• In general ----> 5 days
• Up to 14 days if:
1. Severe infection
2. Slow response to therapy
3. Immunosuppression.
Non-pharmacologic Interventions
Apply warm or, if more comfortable, cool saline
compresses to affected areas QID for 15 minutes.
Mark border of erythema with pen to monitor spread.
Elevate, rest and gently splint the affected limb.
Nursing management
Assess the patient
Objective data
Redness/tenderness Swelling
Warmth on the tisses affected
Nursing Diagnosis
Acute pain related to tissue inflammation as evidenced by
patient’s
verbalization/ body expression/ tarchycardia
Interventions
Rate the pain by the scales
Administer analgesics as prescribed
Use other pain relieving measures such as elevation of limb/
rest the limb
Impaired tissue integrity (subcutenous )related to microbial
invasion as evidenced by swelling, redness and tenderness
Interventions
1. Bacteremia
2. Endocarditis
3. Osteomyelitis
4. Sepsis
LYMPHANGITIS
LYMPHANGITIS
• Acute inflammation of the lymphatic channels.
•Causative organisms- Hemolytic streptococus, staph aureus,
pseudomonas, fungi
Nursing management
Manage Pain, Fever, General
malaise
Lymphangitis can spread quickly, leading
to complications such as:
• Cellulitis
• Bacteremia
• Sepsis,
• Abscess
SEPTICAEMIA
SEPTICAEMIA
• Definition: Infection in the bloodstream also refered to as
bacteremia
Causes
Results from other outbrown focal infections e.g. Lungs, urinary
system or introduced through invasive procedures
CAUSATIVE ORGANISMS
• Staphylococcus
• Streptococcus
• Pseudomonas
• Escherichia coli (E.coli)
Pathophysiology
Entry of bacteria into the blood stream, Triggers an immune
response, inflammatory process, leading to shut down of infection
fighting system and shock then death
CLINICAL MANIFESTATIONS
Early symptoms include:
• Fever/hyperthermia
• Rapid breathing rate (tachypnea) or shortness of breath.
• Rapid heart rate (tachycardia)
• Low blood pressure
• Anxiety
• Reduced urine output/oliguria
• Malaise
• Loss of appetite, nausea and vomiting.
As the septicaemia progresses, the symptoms become more
severe and includes:
• Antibiotics
• Analgesics/Antipyretics
• Blood transfusion if the patient is anemic.
• Oxygen administration
• Fluid replacement
• Provide adequate nutrition
• Preventive measures for pressure ulcers.
PREVENTION
• Can be prevented by appropriately treating the infections which
often precede it. Treat bacterial infections thoroughly to
minimize the risk of spread.
• Good personal hygiene
• Use sterile instruments during invasive procedures.
• Immunize children against Haemophilus influenza B (HIB), and
pneumonia to reduce cases of septicaemia in children.
Medical management
Causes
• Open fire,
• Hot liquds,
• Chemicals
• Electrical causes
Pathophysiology
• After destruction of skin there is a marked loss of fluid from the
body of about 10-20 times more through evaporation and
damage of the blood vessels.
• The trauma of the burn triggers an inflammatory response that
increases vessel permeability leading to increase in fluid loss
(both salt, water and proteins) leading to burn wound edema that
is worst in the first 72hrs
• Loss of skin barrier to microorganisms combined with the
immunosuppression leads to increased bacterial proliferation and
infection with gram +ve and later gram –ve leading to other
infections e.g pneumonia, septicemia and wound infections
Signs and symptoms
Depends with type and degree of burns
Classification
FIRST-DEGREE BURN:
• Confined exclusively to the outer surface and is not considered a
significant burn.
• No barrier functions are altered.
• The most common form is a Sunburn which heals by itself in less
than a week without scar.
Superficial Second-Degree Burn:
• Involves the entire epidermis and no more than the upper third
of the dermis.
• Rapid healing occurs in 1-2 weeks, because of the large amount
of remaining skin and good blood supply.
• Scar is uncommon.
• Initial pain is the most severe of than any other burn, as the
nerve endings of the skin are now exposed.
DEEP SECOND DEGREE BURN:
•Primary survey-
A Airway
B Breathing
C Circulation
D Disability
E Exposure
F Fluid resuscitation
• Secondary survey-mechanism of injury
• Head to toe exam- All body systems
• Burnt surface area
• Burn wound depth
Investigations
• Blood Gas Analysis
• F/hemogram
• Urea/Electrolytes/Creatinine
• LFTS
• Total Protein and Albumin
Treatment
• Fluid resuscitation
• Pain mangement
• Wound management
• Prophylactic antibiotics
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Fluid volume is relatively constant in proportion to the area Of
body burned. Therefore there are formulae that calculate the
approximate volume of fluid needed for the pt of a given Body
weight with a given % of the body burned
2. Hypertonic saline
it produces hyperosmolarity and hypernatremia
Reduces shift of intracellular water to extracellular space
• Colloids have larger molecules, cost more, and may induce allergic
reactions, blood clotting disorders, and kidney failure
Monitoring of resuscitation
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Treating the burn wound
Open method
Silver sulfadiazine application without dressings commonly Used
in burns of face,head and neck.
Closed method
Dressing done to soothen and to protect the wound
To reduce the pain
As an absorbent
44
Dressings
Paraffin gauze
Hydrocolloids ( e.g duoderm)
Full-thickness and deep dermal burns need antibacterial
dressings to delay microbial colonisation prior to surgery
Tangential excision
Can be done within 48 hours with skin grafting in patients with less
than 25% burn
Usually done in deep dermal
burns
Dead dermis is removed layer by
layer Until fresh bleeding occurs
Later, skin grafting done
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Escharotomy
46
A full-thickness burn to the upper limb with a mid-axial escharotomy.
The soot and debris have been washed off.
138
Superficial partial thickness burns
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Superficial partial thickness burn after 3 months
Pigment returning
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Effects of burns
Shock due to hypovolaemia
Renal failure (toxins from burn)
Pulmonary oedema, resp infections, Acute resp. distress
syndrome, resp failure, Infection by staph aureus,
pseudomonas, etc leads to Septicemia
Fungal and viral infections may also occur.
Fluid and electrolyte imbalance.
Immunosuppression predisposes to severe opportunistic
infection.
Eschar formation and its problems e.g. ischaemia when it is
circumferential. (eschar is a dry, dark scab made of dead
skin) 141
Effects of burn (cont…..)
Inhalation burn causes pulmonary oedema, respiratory
arrest
Severe malnutrition with catabolic status,
Toxic shock syndrome: It is a life-threatening exotoxin
mediated disease caused by Staphylococcus aureus. It is
common in children, presents with rashes, myalgia,
diarrhoea, vomiting, and multiorgan failure with high
mortality
Development of contracture is a late problem. It may
lead to disability of different joints, defective hand
functions, growth retardation causing shortening etc
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.
COMPLICATIONS OF BURNS CONTRACTURES
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Complication of contracture
Hypertrophic scar
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Treatment of burn contracture
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Prevention of development of
contracture
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ASSESSEMENT OF TOTAL BODY
SURFACE AREA (TBSA) FOR BURNS
METHODS
i. By depth
ii. Rule of 9 -Estimated percentage of total body surface area (TBSA)
in the adult is arrived at by sectioning the body surface into areas
with a numerical value related to nine. . Head-9%, trunk anterior
and posterior 36%,upper limbs 18%, lower limbs 36%,
gentalia1%. Any burn with above 25% provokes a systemic
response. The patient’s palm for small burns- 1%
iii. Lund and Browder chart – allocates percentage as per the body
anatomical parts.
WOUND HEALING
WOUND HEALING
Wound healing is a mechanism by which the body attempts to restore
the integrity of the injured part.
Systemic factors
• Malnutrition or vitamin and mineral deficiencies
• Disease (e.g. diabetes mellitus)
• Medications (e.g. steroids)
• Immune deficiencies [e.g. chemotherapy, acquired
immunodeficiency syndrome (AIDS)]
• Smoking
Types of wounds
• Surgical- created intentionally to attend to a pathology
• Traumatic wounds- accidental wounds e.g burns, crush, cuts etc
• Chronic – develop due to chronic conditions e.g pressure ulcers,
skin conditions, abscesses etc (more classifications exist)
i) Compensatory stage
• The body tries to compensate for the low blood volume by:
Contactibility of heart
Peripheral vasoconstriction
Reduced urine output
Characterised
by:
Failed cardiac ability of meet the demand and myocardial
ischemia and hypoperfusion of all organs
Systemic vasodilation as a result of release of chemical
mediators into blood stream
Signs and symptoms in this stage:
• Slow heart rate of below 60 beat /min
• Low BP below 90mmhg
• Rapid and shallow respirations
• Crackles due to fluid in the lungs
• Unconcious state
• Stress ulcers may lead to intestinal bleeding
• Signs of acute renal failure
• Raised bilirubin levels
• Low ph
• Jaudice
• Tissue oedema
iii) Irreversible stage
• In CCU setting
•Monitoring – hemodynamic monitoring( ECG, ABGs, renal
function tests Etc)
• Cordination of Collaborative management
• Administration of drugs and fluids
• Family involvement
• Documentation of care
FLUID AND ELECTROLYTE
IMBALANCE
(60% of body wt is made up of fluids )
FLUID AND ELECTROLYTE IMBALANCE
Fluid compartments
Extra cellular
Intravascular
interstitial
Intracellular (within
the cells)
Transcellular –(cerebrospinal, pericardial, synovial,
intraocular, and Pleural spaces)
Third space- abnormal amount of fluid trapped in
peritonial, plueral or other tissues.
• To maintain homeostasis the body regulates the output to match
the input by the renal system, adrenal glands, pituitary glands
( renin, angiotensin II, aldosterone and ADH)
A. FLUID IMBALANCE
CAUSES
3. Dietary management:
Because sodium retention is a primary cause of fluid volume excess,
so sodium restriction diet is often prescribed.
Causes:
• Diarrhea,
• Vomiting,
• Excessive sweating,
• Impaired kidneys,
• Addison’s disease (insufficient production of aldosterone),
• Overuse of diuretics,
• Excess water retention
Effects
• Blood volume is low,
• Hypotention abdominal muscle cramps,
• Nausea,
• Fatigue,
• In severe cases: confusion, muscle twitching and convulsions.
Management
Normal diet with salt if not severe, Iv N/s (restriction of fluids if
causes
related to fluid retention), salt tablets,
• Close monitoring of serum levels
• Management of systemic conditions
Hypernatremia
Caused by:
• Reduced water intake,
• Cushings syndrome,
• Fasting,
• Vomiting,
• Burns,
• Hypertonic solutions such as 4.5% N/S etc
Effects
• Thirst,
• Nausea and vomiting,
• Confusion
• Lethargy and weakness,
• Hallucination in severe cases
• Peripheral and pulmonary edema,
• Postural hypotension
Management
• Treat the cause e.g. Give water or fluids with low sodium
(hypotonic solution) with care not to bring down the levels so fast
which may lead to brain edema.
• Promptly manage systemic causes.
• Monitor the serum sodium levels
Cont’--
Hyperkalemia -
Potassium levels above 5.5 mmol/l
Causes:
• Hemolysis due to trauma,
• Renal failure,
• Acidosis and physiologically after exercises,
• Iatrogenic causes (treatment related, potassium chloride,
heparin, ACE inhibitors, nsaids, and potassium-sparing diuretics)
Effects
• Muscle weakness, at times paralysis,
• ECG changes such as narrow T waves and a shortened QT interval.
• Nausea,
• Diarrhea.
Management
• Fatigue ,
• Anorexia,
• Nausea,
• Vomiting,
• Muscle weakness,
• Leg cramps,
• Paresthesias (numbness and tingling),
• ECG changes - flat T wave
Management
• If not severe, dietary measures could elevate the levels
• If severe ( below 2mmol/l) then intravenous infusions with
potasium is administered with care and should be at 10-
20mmol/hr and not more
• ECG monitoring
• Serum potasium monitoring
Types of imbalances
Acidosis- a state when the PH level in the blood is below 7.3 and
the alkaline buffers eg. Sodium bicarbonate has been used up.
Alkalosis – the ph level of blood is above 7.5 and the acidic reserve is
used up.
The buffer system, kidneys and lungs are unable to contain the
situation of regulating the pH therefore the 2 states develop.
Clinically, the following scenarios are significant:
a) Metabolic acidosis
b) Metabolic alkalosis
c) Respiratory acidosis
d) Respiratory alkalosis
a) Metabolic acidosis
• Can be acute or chronic.
• A state where there is low pH and low bicarbonate in serum
Causes
• Ketoacidosis,
• Lactic acidosis,
• Late phase of salicylate poisoning,
• Uremia
• Methanol toxicity
Signs and symptoms
• Headache,
• Confusion,
• Drowsiness,
• Increased respiratory rate and depth,
• Nausea, and vomiting,
• Peripheral vasodilation
• Decreased cardiac output occur when the pH falls below 7.
Management
Causes
• Gastric fluid loss through vomiting or suctioning,
• Hyperaldosteronism
• Cushing’s syndrome,
• Hypokalemia,
• Long term diuretic therapy,
• Overuse of antacids,
• Chronic ingestion of milk and calcium carbonate.
Signs and symptoms
• Tingling of fingers,
• Depressed respiratory rate,
• Decreased motility,
• Hypertonic muscles ,
• Hypokalemia
Management
• Blood gas analysis – level of ph is increased, the bicarbonate is
high, the CO2 is high since the pt is hypoventilitating
• Restoration of fluid volume
• In order for kidneys to excrete bicarbonate, NaCl is given
• Treat the underlying condition.
c) Respiratory acidosis
•Could be either acute or chronic
•Characterized by pH less than 7.35
Causes
• Conditions that lead to retention of co2 e,g.
• Acute pulmonary edema,
• Obstruction by foreign object,
• Atelectasis,
• Pneumothorax,
• Overdose of sedatives,
• Severe pneumonia
• Acute respiratory distress syndrome
Signs and symptoms
Causes
• Extreme anxiety,
• Hypoxemia,
• The early phase of salicylate intoxication,
• Gram-negative bacteremia,
• Poor setting of mechanical ventilator machine
Signs and symptoms