Author: Claire

Claire Galea is the Owner and Director of Mariposa Holistic Care, through which she provides holistic care services tailored to her clients' personal needs. She is also in her final year following a Degree in Nursing at the Faculty of Health Sciences, University of Malta. Claire is keen about public education on health-related subjects as well as holistic patient-centered care. She is also passionate about spreading positivity and awareness on various subjects through her blog Student Nurse Life.

NPICU – Neonate and Paediatric Monitoring & Central Lines

The first 28 days of life are the most crucial for survival. While on a global scale neonatal mortality is declining, 54% of the total deaths amongst Europe’s children under 5 occur in neonates. This sheds a light on the importance of adequate monitoring and care at the NPICU neonatal and paediatric intensive care unit.

Local causes of mortality in children under 5 years of age include:

prematurity
congenital anomalies
non-communicable diseases (eg. heart disease, cancer, chronic respiratory disease, and diabetes)
birth asphyxia (failure to establish breathing at birth) and trauma
acute lower respiratory infections
sepsis
meningitis

The NPICU – Neonatal & Paediatric Intensive Care Unit

Malta’s only NPICU caters for limitless admissions of neonates and children up to 3 years of age, with the majority of these young patients being premature babies (babies born before the 37th week of gestation) and neonates (from birth to 28 days of age).

Classification of care in the NPICU is as follows:

Intensive Care – 1 or 2:1 care ratio
High Dependency Care – 1:1 care ratio
Special Care – 1:2 care ratio
Nursery – 1:4 care ratio

Apart from being allocated according to experience and training needs, NPICU nurses may need to act as transport team members, Basic Life Support educators, and link nurses.

Why Do Neonates Require Intensive Care?

Maternal Factors

premature membranes rupture
multiple pregnancy
hypertension
diabetes
drug or alcohol exposure
sepsis
bleeding
too much or too little amniotic fluid

Delivery Factors

foetal distress
birth asphyxia
breech delivery
meconium
nuchal cord (umbilical cord wrapped around baby’s neck)
ventouse (vacuum cup) / KIWI (most common type of ventouse that does not use a suction machine)
cesarean

Baby factors

CHANGES AT BIRTH:

independent breathing
foetal to neonatal circulation
metabolic adaptation to thermoregulation, glucose homeostasis, and fluid balance

POST-NATAL CHANGES:

baby’s lungs become the primary respiratory organs
lungs’ blood vessels respond to oxygen increase from vasodilation, promoting blood flow to the lungs
increase in oxygen causes heart ducts to close, leading to neonatal circulation to establish itself

NORMAL CHANGES:

during the baby’s first breaths, air replaces the fluid within the lung

THERMOREGULATORY CHANGES:

at birth, intrauterine heat reservoir and heat exchange through the placenta is lost
following birth, thermal stability is normally achieved independently, as they adapt to the new environment by the non-shivering thermogenesis process
the newborn baby should be kept warm and dry straight from delivery, since becoming cold causes the brown fat stores to become depleted, leading to neonatal hypoxia and hypoglycaemia

GLUCOSE HOMEOSTASIS CHANGES:

at birth, the baby stops obtaining glucose from the mother through the placenta, and starts to produce glucose independently, which, following birth, may cause a decrease in the baby’s blood glucose levels
normally, if kept warm and is fed appropriately within the first few hours after birth, a full term baby is able to control his/her own blood glucose levels within normal limits

FLUID BALANCE CHANGES:

at birth, fluid balance undergoes significant adaptive changes, including extra-cellular fluid contraction following delivery, where neonates may lose up to 10% of their total birth weight

Premature vs Full Term Babies

Premature babies commonly experience respiratory issues, including:

respiratory distress syndrome (due to surfactant deficiency)
chronic lung disease of prematurity (caused by oxygen dependency and persistent inflammatory changes of the lungs past 28 days following birth)
apnoea of prematurity (due to immature brain stem)

NPICU Admission Guidelines

23 weeks-35 weeks or more than 42 weeks gestation
birth weight of 450g – 2kgs, SGA (small for gestational age) and LGA (large for gestational age)
respiratory issues – apnoea, cyanotic episodes, need for positive pressure ventilation, concerning respiratory distress, tachypnoea for over 1hr, perinatal asphyxia, and meconium aspiration
gastrointestinal issues – feeding problems, bile-stained vomiting, signs of obstruction
infection – sepsis suspicion, herpes, chlamydia, group B streptococcus
malformations
congenital heart defects
infants of mothers with diabetes
hypoglycaemia
seizures
surgical complications
neonatal abstinence syndrome – conditions caused when a baby withdraws from certain drugs he’s been exposed to in the womb prior to birth
hyperbilirubinaemia – higher-than-normal amount of bilirubin in the blood, causing jaundice
monitoring

Monitoring

CONTINUOUS MONITORING of:

heart rate
respiratory rate
arterial blood pressure
pulse oximetry
capnography
cerebral function monitoring

INTERMITTENT MONITORING of:

blood gases
serum bilirubin
blood glucose
others as needed eg. haemoglobin, electrolytes, etc.

Central Lines

CVCs (central venous cannulas) can be used for longer than PVCs (peripheral venous cannulas). IV treatments as well as higher concentration IV fluids and TPN can be administered via a CVC with less irritation and damage to the veins.

UMBILICAL CATHETERS

A umbilical cord typically has 2 arteries and 1 vein. Catheters are placed into the blood vessel using sterile technique, followed by a confirmation x-ray to determine position.

An umbilical arterial catheter is used for:

blood sampling
ABGs
invasive blood pressure monitoring
DO NOT ADMINISTER IV FLUIDS IN AN ARTERIAL CATHETER!

An umbilical venous catheter is used for:

IV fluid administration
IV treatment
exchange transfusion
emergency access during resuscitation

Retrieved from https://clipart.me/free-vector/umbilical-cord on 26th January 2023

PICC LINE

A PICC line – Peripherally Inserted Central Catheter – is a thread-like tube which is inserted in a small vein and threaded into a larger vein leading to the Superior Vena Cava.

when handling the baby, the nurse should be extra careful as to not pull the catheter
infusion lines should be carefully changed on alternate days using a sterile technique

NOTE: Neonatal PICC lines SHOULD NOT be used for blood sampling!

TUNNELED LINES

a tunneled catheter is a catheter inserted under the skin, exiting on the chest a.k.a. Hickman
the line is anchored in place by the Dacron cuff, helping to prevent infection

NON-TUNNELED LINES

femoral line
jugular
subclavian
brachiocephalic

INTRA-OSSEOUS LINES

TIVAD – TOTALLY IMPLANTED VENOUS ACCESS DEVICE

Totally Implanted Venous Access Devices are only used in older children
accessed and de-assessed by a certified nurse with a special needle – once needle is in place, it can be used like any other central line

PERIPHERAL ARTERIAL LINES

used for frequent blood sampling
provide accurate invasive blood pressure monitoring
high risk

Retrieved from https://emedicine.medscape.com/article/1999586-technique on 26th January 2023

CENTRAL LINE MONITORING

Central line monitoring is very important since signs and symptoms may be indicating line blockages, vein irritation, thrombus, migration, and CLABSI (central line-associated bloodstream infection). Signs and symptoms that the nurse should watch out for include:

extremity discolouration
bleeding
swelling
extravasation
dislodgement
signs of sepsis

Infiltration – Retrieved from https://europepmc.org/article/pmc/6082416#free-full-text on 26th January 2023

Extravasation – Retrieved from http://www.worldwidewounds.com/1997/october/Neonates/NeonatePaper.html on 26th January 2023

Ischaemia & Necrosis following Peripheral Arterial Cannulation – Retrieved from https://www.semanticscholar.org/paper/Analysis-of-characteristics-of-peripheral-arterial-Kim-Lee/973dec4ffd825f9c336134d16004935b15a83921 on 26th January 2023

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Burn Patient Rehabilitation

Burn patient rehabilitation is both a philosophy and an attitude which needs to start from the day in which the burn injury was inflicted.

Adequate nutrition is one of the most important aspects required for burn patient rehabilitation. Burn patients have increased caloric intake requirements. Lack of caloric intake leads the patient’s body to start metabolising protein, subsequently causing muscle wasting.

Retrieved from https://www.khanacademy.org/science/biology/macromolecules/proteins-and-amino-acids/a/orders-of-protein-structure on 24th January 2023

The Role of Nutrition in Burn Patient Rehabilitation

In patients with a burn injury, feeding should be established as early as possible, and ideally should be administered enterally. The patient’s weight should be monitored, especially since a 10% or more decrease in weight is considered to be a failure. However, it is important to note that while the catabolic state of large burn injuries result in a rapidly falling albumin level causing a decrease in dry weight, this decrease is masked due to the large fluid resuscitation volume administered in the first few days following the injury.

NOTE: patients requiring starvation for anaesthesia should be kept starved for the least time possible, starting from 6hrs pre-anaesthesia administration.

Basal Metabolic Rate – BMR

The Basal Metabolic Rate is the body’s resting rate of energy expenditure. The BMR doubles in cases where the patient has experienced more than 50% TBSA (Total Body Surface Area) burn. The larger the TBSA burned, the higher the hypercatabolism degree (excessive metabolic breakdown of complex substances including protein, within the body). The patient typically also experiences hyperglycaemia resulting as another endocrine response.

Typically, the patient’s BMR continues to increase and the core temperature resets to 1-2°C higher than normal, until the burn wound heals. During this healing process, the ambient temperature should be kept around 26-30°C to reduce the body’s energy demands.

NOTE: TBSA does not take into consideration superficial burns where only the epidermis is involved.

Nutritional Intake During Admission Stage

the patient is weighed so that dry weight measurement is established and recorded
a nasogastric tube is inserted, and feeding is started at low volume
feed volume is gradually increased if the nurse determines that the feed is actually being absorbed

Caloric requirements are calculated by a dietician based on the TBSA burned. In burn patients the Curreri formula is used to determine nutritional intake requirement:

The Curreri Formula

(25 x weight in kg) + (40 x TBSA percentage)

Enteral Feeding

studies show that patients receiving enteral feeding have a decreased mortality and morbidity rate
enteral feeding is relatively easy to establish early on, and this helps decrease caloric deficit
in patients with extensive burns obviously requiring a longer hospital stay, a PEG or nasojejunal tube is recommended, since this helps avoid repeated periods of starvation, and can also be passed at the bedside; since by using this way of feeding, nutritional intake bypasses the stomach and goes directly into the intestines, the patient would not require starvation pre-anaesthesia
PEG feeding is used less in burn patients, especially if the abdomen has suffered from a burn injury, or if the abdominal skin may be required as donor skin
Total Parenteral Nutrition TPN is only indicated if enteral feeding cannot be established, since studies have shown an increase in burn mortality with IV supplemental feeding in severely burned patients; additionally, due to an increase in burn patients’ core temperature, phlebo-fix used to hold in place a central line tends to keep coming off, thus, a central line is ideally avoided

Retrieved from https://healthcarenutrition.org/methods-of-nutrition/ on 24th January 2023

Retrieved from https://www.myupchar.com/en/surgery/percutaneous-endoscopic-gastrostomy-peg on 25th January 2023

Burn Patient Co-morbidities

A burn patient may have other primary diseases such as diabetes, high cholesterol, and obesity. Such diseases are referred to as co-morbidities. For this reason, every burn patient needs to be managed in a holistic way, where all pre-existing medical conditions, any related social circumstances, and obviously the patient’s age, are taken into consideration when drawing a burn patient rehabilitation plan.

Diabetes

diabetes affects the healing process of the burn injury due to poor circulation leading to less oxygen perfusion
burn wounds, like any other wound, is likely to become infected in a patient with diabetes, thus, patients with diabetes are frequently checked for microbe presence by wound swabbing
careful monitoring and control of blood glucose levels in patients with diabetes promote better clinical outcomes, therefore this should be monitored right from admission stage
antibiotic administration is likely to help improve graft take as well as healing period in patients with diabetes
upon admission of a diabetic patient with a burn injury, the diabetic liaison nurse should be informed

Obesity

obesity limits burn injury outcome in various ways
typically, the force of abdominal viscera on the diaphragm limits lung tidal volumes

Age

young burn injury patients are quite resilient especially since their skin is relatively thin but the ratio of their skin surface area to blood volume is relatively high
elderly patients have very thin skin, and so, burn injuries endured by patients over 65 years of age are typically classified as full thickness burns; superficial burns in the elderly tend to progress to full thickness burns due to lack of nutrition, lack of self care, and sluggish circulation

Burn Reconstructive Procedures

Reconstructive procedures are performed following burns as well as cancer tumour removal. Plastic surgery uses the Aucher classification to classify burn reconstructive procedures according to their urgency. Burn reconstruction involves scar release or excision. Closure is done either by using a normal flap or by recruiting local skin.

Primary Intention Burn Injury Healing – done through surgery; surgery however doesn’t restore sensory functioning
Secondary Intention Burn Injury Healing – done through normal wound healing, with dressing changes as required and antibiotics to avoid infection; normal wound care without plastic surgery tends to lead to contractures that limit the patient’s functionality

An injury in which part of the body is lost eg. dog bites, human bites, woodwork injuries, butchers etc, is ideally subjected to secondary intention healing, since unintentionally closing the wound with microbes inside may lead to infection and subsequent surgical reconstruction or possibly amputation.

burn patient rehabilitation — Skin Contractures – Retrieved from https://link.springer.com/chapter/10.1007/978-3-030-44766-3_13 on 25th January 2023

Skin Grafts

A skin graft is a surgical intervention in which tissue is moved from one area (donor site) to another (recipient area). The donor area can be either from the same body or from another.

FULL THICKNESS SKIN GRAFTS

include the epidermis and dermis
full thickness grafts can be harvested from only a few body sites
may be used to cover bone exposure
donor sites require direct closure or split thickness graft closure
uptake rate is higher than that by split thickness grafts since the dermal layer is involved
antibiotics are administered as prophylaxis to avoid infection of skin grafts

SPLIT THICKNESS GRAFTS

include the epidermis and less than the whole thickness of the dermis
is commonly done for acute burn wound closure
healing is done through secondary intention
uptake rate is less than full thickness skin grafts since only the epidermis is involved, and this is mashed, causing fenestrations in the graft area, and is also quite stretched

Care of Grafts

foam is usually sutured or stapled over the graft to increase pressure
foam is removed after 5 days so that the graft is reviewed
graft is covered with antibacterial dressings
alternate removal of staples from graft is carried out after 2 days

Care of Donor Site

following harvesting of the skin, the donor site is covered with an alginate dressing (kaltostat) to control bleeding and protect the wound from becoming infected through contamination
donor site is exposed after 15 days so as to minimise bleeding; DO NOT REMOVE, even if bleeding is noted – remove ONLY if the wound becomes very smelly, signalling infection

Flaps – Local and Distant

flaps refer to the transferring of tissue that contains its own blood supply since vascularity is moved along with the flap during surgery
local flaps have some continuity with the defect they cover
distant flaps are separated by distance through the use of micro-surgery
flaps need to be kept warm at all times

The difference between grafts and skin flaps is in the fact that grafts do not bring their own blood supply, however, skin flaps carry their own blood supply to the recipient area.

Care of Flaps

flaps are held in place by staples or sutures
removal of staples or sutures is done based on the surgeon’s advice

NOTE: NEVER apply pressure over the flap since this impedes circulation to the area, causing flap necrosis.

Burn Patient Rehabilitation Into Society

Burn injuries have comprehensive needs which are best treated with adequate resources. This is why a multidisciplinary team, commonly managed by a lead consultant, is involved in the burn patient rehabilitation process.

Physiotherapy

physiotherapy is focused on the anatomical and physiological factors related to patient rehabilitation, helping in preventing or treating impairments or disabilities
physiotherapy promotes exercises aimed at regaining strength, range of motion, and stretching of the scar area
physiotherapy may also include chest physio which helps during the healing process, especially in patients who were exposed to smoke inhalation

occupational therapy

occupational therapy focuses on the functional aspect of the patient’s ability to participate in the daily activities of life, providing functional training to promote improvement
occupational therapy helps prepare the patient for discharge in relation to required support and services, including necessary equipment and environmental adaptations, assessment and provision

Burn Patient Challenges Prevention

Burn patients may experience various challenges during their healing process, some of which may result in disabling and disfiguring contractures. Challenges may include:

pain
scarring
acute and/or chronic oedema
muscle wasting (caused by immobilisation and long periods of reduced functionality)
psychological pain caused by trauma and body image changes
physical, mental and social limitations when compared to pre-injury

There are things we can do or promote as nurses so as to decrease or ideally prevent such challenges. These include:

educating, motivating, and empowering the patient through promoting understanding of the healing process
positioning the patient in a way as to protect the joints, reduce pressure, immobilise, and decrease oedema
splinting to protect, immobilise, prevent contractures and regain range of movement
chest physiotherapy helps in secretion removal whilst increasing tidal lung volume
promoting passive, active, and active assisted exercises to prevent loss of range whilst strengthening the muscles
scar massage, silicone, and pressure garments

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Burn Injury ~ Types of Burns & Treatments in Critical Care Setting

A burn injury happens when the skin comes into contact with something hot, causing disruption within the skin’s cell structure, resulting in skin cell death.

NOTE: Throughout this blogpost, the various burns listed are classified into burn degrees, however, this method of classification does not indicate the injury depth, and so, focus should be on the type of burn eg. superficial burn, and the percentage of skin area affected using the Lund and Browder Chart (featured further down).

The Zone of Stasis

The Zone of Stasis is the surrounding area of the burn. It is characterised by decreased tissue perfusion. Nonetheless, the skin within this zone is potentially salvageable:

the burn injury dressing should be chosen with the aim of promoting wound moisture
burnt area should be elevated so as to minimise oedema
smoking should be avoided by the patient since it puts the patient at increased risk of poor outcomes and complications
systemic diseases eg. diabetes should be managed; blood sugar levels should be kept stable

Assessing Burn Injury Surface Area

Prior to assessing a burn injury and its depth, DO NOT apply any silver sulfadiazine or any other topical agents, since doing so gives an inaccurate indication of the wound’s depth.

Retrieved from https://www.theplasticsfella.com/total-body-surface-area-in-burns/ on 22nd January 2023

Superficial Burn Injury

A superficial burn, also called a 1st degree burn, is characterised by the following features:

painful
no blisters are present
only the epidermis layer is involved
erythema (redness) present due to vasodilation
complete healing typically takes up to 7 days due to re-epithelialisation

Care of Superficial Burn

superficial burns require no dressings
patient should be advised to apply emollient cream
patient should be advised to apply sunblock and to avoid the sun

Superficial Partial Thickness Burn Injury

A superficial partial thickness burn, also called a 2nd degree burn, is characterised by the following features:

very painful
pink or red
blisters present
wet and weepy
complete healing with relatively little scarring

Care of Superficial Partial thickness Burn

if available apply Aquacel (silver dressing) in the 1st 24 hours following injury
de-roof and debride the blisters UNLESS they are located on the palms or soles of the feet due to excessive pain as well as superficial nerves, to which debridement may cause irreparable problems
assess wound depth
apply silver sulfadiazine and cover with non-adherent dressing for the first 3 days following burn injury
advise patient that a lot of exudate is expected to come out from the wound
advise patient to take regular analgesia for pain management

Deep Partial Thickness Burn Injury

A deep partial thickness burn, also called a 3rd degree burn, is characterised by the following features:

usually lacks physical sensation
red with overlying eschar
scarring expected
delayed healing potential

Care of Deep Partial thickness Burn

de-roof and debride blisters (if any) UNLESS they are located on the palms or soles of the feet due to excessive pain as well as superficial nerves, to which debridement may cause irreparable problems
assess wound depth
apply silver sulfadiazine and cover with light dry dressing
inform patient that some exudate should be expected
advise patient to take regular analgesia for pain management

Full Thickness Burn Injury

A full thickness burn, also called a 3rd or 4th degree burn, is characterised by the following features:

lacks physical sensation
white, brown, tan, or black
dry and leathery
firm non-blanche
scarring expected
no healing potential

Full Thickness Burn Injury 3rd Degree Burn (Left) and 4th Degree Burn – Retrieved from https://www.capersonalinjurycaselawnotes.com/2009/06/burn-injuries/partial-thickness-and-full-thickness-burns/ on 22nd January 2023

Care of Full Thickness Burn

following diagnosis of burn wound stage, refer patient to the Burns Unit
apply aquacel
elaborate surgical debridement, reconstruction, or amputation, may be indicated, depending on the case

Thermal Burns

The WHO estimates that thermal burns account for around 6.6 million injuries and 300,000 deaths yearly, worldwide. A thermal burn can be experienced through the following:

scalding (commonly caused by hot drinks in children)
direct contact with hot materials
flash and flame burns
can be a 1st, 2nd, 3rd or 4th degree burn (most full thickness burns are classified under thermal burns)

1st, 2nd and 3rd Degree Thermal Burn – Retrieved from https://burncenters.com/burns/burn-services/thermal-burns/ on 22nd January 2023

Chemical Burns

Chemical burns can be caused by direct contact with, or fumes of a chemical, usually an alkali or a strong acidic substance. Such burns can happen within various settings, including homes, work, or during an assault.

One such commonly used chemical is hydrofluoric acid – a colourless highly corrosive solution containing hydrogen fluoride in water. It is stored in a plastic container and is commonly used in industrial chemistry, glass finishing, and cleaning. Liquid hydrofluoric acid has the potential to interfere with calcium metabolism. It can cause deep skin burns, which though initially painless, may lead to a cardiac arrest and subsequent death, whilst in gas form, it can cause immediate and permanent lung damage, as well as damage to the eyes’ corneas.

care of a chemical burn

A chemical burn requires special care and attention so as to stop the substance from spreading within the skin. When caring for a chemical burn:

obtain information as to what caused the chemical burn
obtain information on how long the area was exposed to the chemical
remove any contaminated clothing that the patient may still be wearing
wash area to dilute or remove the substance
keep the wound under running water for 20 minutes

Smoke Inhalation

Smoke inhalation, which includes inhalation of heat, chemicals, and soot, can lead to a burn injury to the airway. To confirm smoke inhalation, it is important to assess for:

burns in mouth area
sooty sputum
voice change
difficult cough

If in doubt one should still provide oxygen therapy following intubation whilst protecting the cervical spine.

TREATMENT

Based on the inhalation severity:

patient may be intubated for minimal upper airway swelling
if soot is present in large amounts, patient’s airway may need suctioning
if the respiratory tract requires support, an aggressive approach should be taken…
chest physiotherapy
bacteriological surveillance – prophylactic antibiotic is administered
administration of The Galvenstone Protocol: inhaled H1 blockers, inhaled heparin, and nebulised acetyl cysteine

Electrical Burns

Electrical burns are caused by exposure to an electric source. They typically have both an entry and an exit site. The extent of such an injury ranges from minimal injury to severe multi-organ involvement.

An electrical burn needs to be evaluated by a medical professional despite the patient’s condition, be it stable or not.

Radiological Burns

Radiological burns are caused by the exposure to radiation. Whilst the most common cause of a radiation burn is through UV radiation as sunburn, patients undergoing radiation may present with radiation ulcers following radiotherapy, which unfortunately increases cancer risk and causes cell death.

Burn Injury Nursing Care

A patient with burns is ideally kept in a positive-pressure room when hospitalised. Positive-pressure rooms have higher air pressure than the adjoining areas, preventing airborne pathogens from entering the room to avoid the air inside becoming contaminated. This reduces the risk of burn patients acquiring infection and causing further complications in their healing process.

Shock and Fluid management

In patients with critical burns, shock causes progressive failure of the circulation, leading to a decrease in oxygen perfusion within the vital organs. Fluid resuscitation aims to:

maintain vital organ function especially when it comes to renal function
replace fluid lost within the first 8 hours following burn infliction

Fluid Resuscitation Formula – Hartmann’s

4ml x weight x affected Total Body Surface Area (TBSA)

to be administered over the first 24 hrs

(Half of the prescribed volume should be administered over the first 8 hours from burn infliction, with the rest over the following 16 hours)

CRYSTALLOIDS VS COLLOIDS

The most commonly used resuscitation fluid for initial resuscitation is the Ringer’s Lactate (Hartmann’s) or other crystalloids. Crystalloids make up a balanced solution which helps balance electrolytes in large fluid replacements.

When compared to colloids, crystalloids have a less prominent affect of volume expansion, however colloids tend to exacerbate third space losses. In burn patients, colloids (commonly used being albumin) are added to decrease the total volume of resuscitation fluid needed, since these reduce capillary leakage. Albumin is however commonly used as a rescue approach since it increases mortality in critically ill patients. Albumin:

reduces fluid creep (fluid overload)
tends to cause haemodynamic instability – hypotension, oliguria, and increasing haematocrit

If Albumin is indicated as an adjunct to the fluid resuscitation protocol, it should replace HALF of the crystalloid amount.

URINE OUTPUT

Urine output is vital for indicating successful fluid resuscitation. A urine catheter should be inserted whenever fluid resuscitation is being performed, since in burn patients, the nurse needs to monitor:

urine output
heart rate
blood pressure
ABGs
pH (patient may experience lactic acidosis)

Expected Urine Output in Patients Undergoing Fluid Resuscitation:

Adults: 0.5ml/kg/hr

Children: 1.0ml/kg/hr

NOTE: fluid resuscitation increases oedema. Fluid formulae should only be used as guidelines, and fluid calculations need to be calculated from the time at which the burn was inflicted. Ideal fluid resuscitation should include the LEAST amount of fluid necessary to maintain tissue perfusion, maintain vital physiological functions, and return physiology to normal as soon as possible.

Retrieved from https://slideplayer.com/slide/13463859/ on 23rd January 2023

THE GASTROINTESTINAL SYSTEM OF A PATIENT WITH BURNS

In burn patients, the liver’s function forms part of the systemic response to the burn injury, excreting glucagon and inflammatory markers.

Secondary Abdominal Compartment Syndrome (SACS) is a common crystalloid resuscitation complication caused by increased intra-abdominal pressure which may cause a secondary organ infarction if ignored. Typically, a patient with SACS has reduced urinary output which may also be bloody.

To avoid SACS, the patient’s intra-abdominal pressure should be measured, either via the patient’s bladder, or by measuring the intra-vesical pressure.

cleaning the burn Injury

a new burn is considered to be sterile, thus, it is important to attempt to keep it that way
clean thoroughly with an antibacterial wash eg. betadine surgical scrub
antibiotics should not be prescribed as prophylaxis, but only if infection is noted (a temperature of up to 38.5°C is considered to be normal in patients with burn injuries)
de-roof and debride large blisters UNLESS they are located on the palms or soles of the feet due to excessive pain as well as superficial nerves, to which debridement may cause irreparable problems
debride any dead skin to promote healing

Change of Dressings

in the initial stage, dressings should be changed daily, especially since at this stage these are usually found soaked
once healing starts to progress, change of dressing should be performed every 3-5 days, however, if the wound becomes painful, smelly, or soaked at any time, it should be immediately changed

Further care

encourage daily moisturiser application eg. aqueous cream
encourage sunblock use over healed areas for 6-12 months
advise patient that pruritus is a common problem following burn injury, and that advise should be sought if this becomes problematic
provide patient with support and reassurance, without any false hopes

NOTE: unhealed burns lasting 3 weeks should be referred to the Burns Unit.

Renal Failure

Renal failure in a patient with burns is usually a late septic complication, especially since within the acute stage the patient would be receiving aggressive fluid resuscitation. To avoid such complication, haemofiltration is commonly considered in large burn injuries. Renal failure signs include:

oliguria of <4o0ml per day
a decline in the GFR
a rise in Urea and Creatinine

A patient needing kidney relief may be put on the PrismaFlex System.

Patient Education on Burns First Aid Care

always aim to stop the burning process by removing the heat source and any affected clothing
if clothes catch on fire, “STOP, DROP & ROLL”
put burn wound under running water for 20 minutes following a burn injury
protect the burn by covering it with a sterile non-adhesive bandage
manage pain through analgesia eg. paracetamol
DO NOT use ice water since this causes vasoconstriction, leading to burn progression
DO NOT apply any creams or ointments to burn injuries since these may cause further complications

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Hypovolaemic Shock

Shock can be classified into 3 different types: Hypovolaemic Shock, Cardiogenic Shock, and Septic Shock. Whilst the management of shock varies based on the type of shock it is, the resulting effect of all 3 types of shock is the same – decreased tissue perfusion.

Features of a Hypovolaemic Shock

Hypovolaemic shock is the most commonly occurring type of shock, which is also easily reversible if treated in a timely manner. Features of a hypovolaemic shock include:

loss of circulating or intravascular volume
impaired tissue perfusion
inadequate delivery of oxygen and nutrients
may be caused by relative and absolute hypovolaemia, or loss of blood or other fluids

Absolute Hypovolaemia

The phrase Absolute Hypovolaemia refers to external loss of fluids from the body. Fluid loss may be that of whole blood (through trauma or major surgery), loss of plasma (through burns) and loss of other fluids such as massive diuresis (through skin loss), severe vomiting, diarrhoea, and dehydration (through diabetes insipidus – a rare condition unrelated to type 1 or 2 diabetes which causes diuresis and polydipsia, diabetic ketoacidosis, and HONK – hyperglycaemic hyperosmolar non-ketotic coma – coma resulting from very high blood glucose levels in a patient with normal ketone levels; very high blood glucose levels combined with high ketone levels may be due to ketoacidosis).

Internal Haemorrhage

Internal Haemorrhage may be caused by:

fractures
GI bleeding
organ rupture (eg. spleen, liver, and kidneys)
pregnancy complications (eg. ectopic pregnancy or post-partum haemorrhage)

Fluid Loss – from intravascular space to extravascular space – may be caused by:

burns
pleural effusion
peritonitis – inflammation of the peritoneum
pancreatitis – inflammation of the pancreas
ascites – a condition in which fluid collects in spaces within the abdomen

Pathophysiology of Hypovolaemic Shock

relative or absolute hypovolaemia
decreased circulating volume
decreased venous return (decreased preload)
decreased stroke volume
decreased cardiac output
decreased cellular oxygen supply
impaired tissue perfusion
impaired cellular metabolism

Signs & Symptoms

impaired consciousness
pale, cool, clammy extremities
prolonged capillary refill time
increased heart rate
increased respiratory rate
hypotension (SBP <90mmHg & reduced pulse pressure SBP-DBP)
reduced urine output
metabolic acidosis
signs of bleeding (decreased Haematocrit & Haemoglobin)

hypovolaemic shock — Retrieved from https://twitter.com/misirg1/status/1382458804995035144 on 19th January 2023

Management

Identify & Treat the Underlying Cause
Restore Intravascular Volume & Blood Pressure
Redistribute Fluids to Ensure Perfusion
Prevent Shock Progression
Avoid onset of Cardiogenic Shock

stop the bleeding by applying pressure to injured site and prepare patient for surgery
administer antiemetics for severe vomiting, antidiarrhoeal agents to treat diarrhoea, insulin for dehydration caused by diabetes, and desmopressin for diabetes insipidus
establish good venous access through large peripheral lines and central venous catheters
insert a urinary catheter to monitor renal perfusion and fluid balance
monitor haemodynamic parameters and the patient’s condition, and titrate fluid administration according to patient’s needs
crystalloids are electrolyte solutions such as Isotonic (eg. normal saline or RLactate), Hypertonic (eg. 10% Dextrose) or Hypotonic (eg. 0.45% NaCl – Sodium Chloride); these address both fluid and electrolyte loss
colloids include blood and its products such as Fresh Frozen Plasma (FFP), as well as synthetic plasma expanders such as Gelafundin (a colloidal plasma volume substitute in an isotonic balanced whole electrolyte solution that can be used for prophylaxis and therapy of hypovolaemia and shock); ADVANTAGES: colloids remain in the intravascular space, restoring fluids faster and with less volume, while blood restores Hgb; DISADVANTAGES: colloids are expensive, may cause reactions, and may also leak out of damaged capillaries, causing additional problems including cardiac failure and peripheral oedema
based on the patient’s blood group and cross match, administer infusions of packed red blood cells to increase circulatory volume and oxygen carrying capacity; fresh frozen plasma, platelets, and cryo precipitate (the insoluble portion, or precipitate, that remains when the liquid portion of the plasma drains away) may also be indicated – blood products are commonly administered through a blood warmer so as to prevent or manage hypothermia
during surgical procedures such as cardiothoracic surgery, chest and abdominal trauma, and orthopaedic surgery, the patient can receive own blood through the intra-operative blood salvage machine, which collects lost blood through a filtered tube and readministers it within 4 hours; this reduces the risk of reactions and infections, however, it does carry an increased risk of haemolysis and microemboli formation during the collection and administration period
pay attention to any arising complications of fluid administration eg. allergic reactions and infection, electrolyte imbalance, dilution of haemoglobin and clotting factors, and pulmonary oedema (higher risk in older adults, and patients with chronic heart failure or renal failure); monitor patient’s urine output and fluid balance, haemodynamic monitoring, fluid responsiveness, and lung sounds
haemorrhagic stroke drug therapy may include inotropes and vasopressors (typically adrenaline or noradrenaline and dobutamine) to increase cardiac output and blood pressure for better perfusion; these however increase oxygen demands; ensure secure airway and administer oxygen if needed to treat hypoxia; antifibrinolytics such as tranexamic acid may be required to prevent the breakdown of fibrin, which is the main protein in a blood clot

Retrieved from https://www.getdoc.com/blood-type-basics-blood/ on 19th January 2023

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Septic Shock

Distributive Shock

impaired distribution of circulating blood volume
vasodilation
capillary leaks

Distributive Shock is sub-classified into 3 other types of shock: septic shock, anaphylactic shock and neurogenic shock. In this blogpost we will be focusing on Septic Shock.

Septic Shock

While sepsis is defined as a life-threatening organ dysfunction caused by dysregulated host response to infection, a septic shock is defined as a subset of sepsis in which underlying circulatory, cellular and metabolic abnormalities and profound enough to substantially increase the risk of mortality.

microorganism entry into the patient’s body
dysregulated host response characterised by excessive peripheral vasodilation, causing maldistribution of blood volume, over-perfused peripheral areas and under-perfused central areas
is the major cause of admission in the critical care setting

Septic Shock may originate from the community (>80% of cases) or during a stay in a healthcare facility. Common sites for origin of septic shock include:

lung
abdomen
bloodstream
renal
gastrointestinal tract
bone
soft tissue
surgical wounds

Infective organisms may include:

Gram negative bacteria eg. Klebsiella, Escherichia coli, and Pseudomonas aeruginosa
Gram positive bacteria eg. Staphylococcus aureus and Streptococcus pneumoniae
Viruses
Fungi
Parasites

Predisposing Factors

Intrinsic Factors	Extrinsic Factors
age extremes	invasive devices eg. catheter use
malnutrition	immunosuppressing drug therapy eg. steroids
co-existing diseases eg. malignancies, AIDS and Diabetes	immunosuppressive therapy eg. chemotherapy
	wounds
	surgical or invasive procedures

NOTE: all critically ill patients are at an increased risk of developing septic shock.

Septic Shock Signs & Symptoms

general malaise
fever OR hypothermia
tachycardia
tachypnoea
altered mental status
hypotension
impaired gas exchange
mottled skin
prolonged capillary refill
oliguria – urinary output less than 400 ml per day or less than 20 ml per hour

Investigations

CBCs
ABGs
c-reactive protein
clotting profile – prothrombin time and INR
urea & electrolytes
liver function tests
urinary function tests
serum lactate – helps identify cryptic septic shock

Septic Shock Diagnosis

Rapid recognition and resuscitation is crucial for survival, and so, deteriorating patients should be investigated for infection in a timely manner.

Sepsis	Septic Shock
presence of infection	adequate fluid resuscitation not enough
acute change in SOFA score of 2 points or more from baseline	vasopressors required to keep MAP at >65mmHg and Serum Lactate at >2mmol/L

Sequential Organ Failure Assessment Score (SOFA)

SOFA is a bedside tool that helps identify patients with infection at an increased risk of death or prolonged ICU stay. SOFA is considered to be positive when the patient has at least 2 of the following 3 criteria:

respiratory rate of >22 breaths/minute
altered mental state with a GCS <15
systolic blood pressure <100mmHg

septic shock — Retrieved from https://www.crit.cloud/summaries–reviews/the-bat-and-the-sofa-the-3rd-consensus-definitions-for-sepsis-are-out on 20th January 2023

Multiple Organ Dysfunction Syndrome (MODS)

MODS refers to a clinical syndrome characterised by acute potentially reversible dysfunction of two or more organs or organ systems not directly involved in the primary disease process. It is the ultimate complication of Septic Shock.

Airway Support

stabilise the patient’s airway
maintain oxygen saturation >94% (unless patient has COPD)
mechanical ventilation may be required to improve oxygenation and neutralise metabolic acidosis

Identifying Source of Sepsis + Treatment

Microbiology – blood, sputum, CSF, urine, wound swab specimens should be sent immediately for Culture & Sensitivity (2 sets of blood cultures should be taken, the 2nd one being with increased sensitivity for detecting bacteraemia); IMPORTANT: take cultures BEFORE antibiotics are administered (even though broad antibiotics should be started within 1 hour)!
Radiology – x-ray and CT scan should be performed to check for signs of infection

IV Antibiotics – start broad spectrum IV antibiotics within one hour to cover likely causative agents such as resistant organisms like MRSA, VREs and Klebsiella, or endogenous infections by colonising bacteria
Adjust Antibiotic Regime – upon identification of specific pathogens
Eliminate Sepsis Source within 12 Hours – debride any infected or nectrotic tissue, drain abscesses and secretions, and remove infective invasive devices

Fluid Resuscitation

Fluids are required to counteract absolute hypovolaemia (sweating, diarrhoea, hyperventilation) and relative hypovolaemia (vasodilation and peripheral blood pooling).

start crystalloids within one hour using the fluid challenge – 30ml/kg over 3 hours, titrating according to response
if necessary, colloids may be administered to patients who had to receive large volumes of crystalloids
CAUTION: watch out for fluid and chloride overload

Inotropes and Vasopressors

If fluid administration is unsuccessful in maintaining physiological parameters and adequate perfusion (MAP should be maintained at >65mmHg), or in the case of myocardial dysfunction, inotropes and vasopressors may be required.

administer noradrenaline to revere inappropriate vasodilation, lower risk of tachycardia and arrhythmias with less adverse metabolic effects
adrenaline may also be added as an adjunct if required
dobutamine may also be added if the patient remains unstable; this may also help counteract excessive vasoconstriction, especially within the peripheries

Corticosteroid Use

corticosteriods (hydrocortisone 200mg/day) may be indicated due to their anti-inflammatory effects in patients unresponsive to fluids and vasopressors NOTE: corticosteroids should not be discontinued abruptly!

Nutrition

nutritional support is particularly important for patients with septic shock since this helps improve their immune response
in case of patients with wounds, a high protein diet is recommended since it helps speed up the healing process
maintain the patient’s blood glucose level at <10mmol/L but avoid excessive glucose control to prevent hypoglycaemia

General Support

maintain temperature control to decrease metabolic demands
provide skin care and pressure ulcer prophylactic measures
provide prophylactic therapy to prevent venous thromboembolism
prevent over-sedation
aim to prevent ventilator-acquired pneumonia and infections related to lines/catheter use
provide blood transfusions only if the patient’s Hgb is <7mmol/L, or in case of bleeding, myocardial ischaemia, and severe hypoxia

Give high-flow oxygen via non-rebreathe bag. Take blood cultures and consider source control. Give IV antibiotics according to local protocol. Start IV fluid resuscitation Hartmann’s or equivalent. Check lactate. Monitor hourly urine output consider catheterisation. within one hour….plus Critical Care support – Retrieved from https://slideplayer.com/slide/12865670/ on 20th January 2023

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Cardiogenic Shock

impaired ability of the heart to pump blood as it should (left or right ventricle dysfunction), causing systemic hypoperfusion and tissue hypoxia
may be caused by cardiac injury (eg. cardiac tamponade), cardiopulmonary arrest, following cardiac surgery, dysrhythmias (severe tachycardia or bradycardia), myocardial tissue necrosis following a Myocardial Infarction, or structural problems (eg. valvular damage or regurgitation, pulmonary embolus, acute myocarditis, papillary muscle rupture, intracardiac tumour, and congenital defects
compensatory mechanisms may worsen the situation…eg. reduced cardiac output due to myocardium death causes increased contractility which further increases the heart’s workload and oxygen demand; reduced blood pressure causes the release of catecholamines which leads to vasoconstriction, subsequently leading to a further increase in cardiac workload and oxygen demand

Cardiogenic Shock Signs & Symptoms

chest pain or chest trauma
altered level of consciousness
cool, pale moist skin
weak thready pulse
tachycardia possibly with dysrhythmias
tachypnoea
SBP <90mmHg and MAP 30mmHg less than normal
urine output <30ml/hr
jugular venous distension
reduced cardiac output and cardiac index
increased PAWP (Pulmonary Artery Wedge Pressure), increased RA (right atrium) pressure & increased SVR (systemic vascular resistance)
signs of pulmonary oedema eg. hypoxaemia, crackles, and frothy sputum

Management

Treat Underlying Cause to Prevent Further Damage & Preserve Healthy Myocardium
Enhance Pumping Effectiveness by Increasing Cardiac Output
Improve oxygen perfusion in the heart as well as other organs and tissues
Increase oxygen supply and reduce oxygen demand of the heart

provide oxygen therapy through supplementary oxygen or mechanical ventilation due to cardiac ischaemia and chest pain
administer morphine for analgesia and sedation, and promote rest
if patient has pulmonary oedema, administer diuretics eg. furosemide or bumetanide, and oxygen whilst monitoring haemodynamic status and ABGs of the patient; diuretics reduce fluid accumulation which causes a decrease in preload – monitor for fluid and electrolyte imbalance
provide mechanical reperfusion through PCI (percutaneous coronary intervention) eg. angioplasty and coronary stents, or a coronary artery bypass graft (CABG)
provide thrombolytic therapy through pharmacologic agents eg. streptokinase, urokinase, tissue plasminogen activator TPA, which dissolve clots in coronary artery BEFORE cardiogenic shock sets in; ATTENTION: watch out for bleeding!
provide drug therapy that helps improve cardiac output by increasing cardiac contractility, decreasing preload and afterload, and stabilising the heart rate
provide fluids with great caution since this increases risk of pulmonary oedema
administer inotropes (eg. dobutamine or milrinone) to improve contractility and reduce afterload, and vasopressors (eg. adrenaline or noradrenaline) to increase contractility, vasoconstriction, blood pressure, and heart rate NOTE: inotropes and vasopressors can be given in combination
administer vasodilators eg. nitrates to reduce oxygen demands by reducing preload through venous dilation, reducing afterload by arterial dilation due to less resistance, increasing oxygen supply to the myocardium due to coronary vasodilation, but ATTENTION – vasodilators cause hypotension!
treat arrhythmias with anti-arrhythmic drugs eg. amiodarone to help increase time for ventricular filling
make use of the intra-aortic balloon pump – a long balloon attached to a large bore catheter inserted through the femoral artery to the descending aorta, with the balloon tip placed just below the aortic arch, and the bottom tip above the renal artery; the attached machine helps by inflating the balloon with helium at the start of diastole when the aortic valve closes, and rapidly deflating it at the start of ventricular systole, just before the aortic valve opens; ATTENTION to possible complications eg. dislodgement of clots, limb ischaemia / neuropathy (check pedal pulses), bleeding (check clotting time before insertion and removal), infection, balloon rupture, and improper position
if indicated, the Left Ventricular Assist Device may be used – flow pump which is placed across the aortic valve into the left ventricle; it draws blood continuously from the left ventricle to the proximal aorta; may be used prior to transplantation or long term for transplantation-ineligible patients
the VA-ECMO is a device through which deoxygenated blood is drained through the central vein; blood is then oxygenated outside of the patient’s body, before being returned through the large artery; it helps improve aortic flow and organ perfusion, however, it may increase afterload and worsen pulmonary oedema; note increased risk of acute kidney injury, severe bleeding, lower limb ischaemia, and stroke
if indicated, a patient with cardiogenic shock may undergo surgical interventions such as human heart transplantation, repair of septal, ventricular, or papillary muscle rupture, or valve repair or change

Retrieved from https://www.magonlinelibrary.com/doi/abs/10.12968/bjca.2021.0055?journalCode=bjca on 20th January 2023

Cardiogenic Shock and Intra-aortic Balloon Pump => https://www.youtube.com/watch?v=mADxD7C8jBw

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Shock Nursing Management – Assessment, Diagnosis & Care

Shock nursing management depends on the accurate and timely identification of shock. This can be obtained through an accurate assessment, thorough investigations, and a proper diagnosis, following which, the right treatment and requirements can be planned and provided to the patient.

Assessment

When assessing for shock, one should keep in mind that clinical changes are initially quite subtle. Still, the following aspects must be taken into account during an initial patient assessment…

patient history
level of consciousness
signs of internal or external bleeding
skin colour and/or moisture
respiratory rate and effort
heart rate and rhythm
body temperature
blood pressure
urine output

shock nursing management — Retrieved from https://www.grepmed.com/images/4224/types-table-signs-classification-symptoms on 16th January 2023

Investigations

Clinical tests should be carried out to confirm shock and identify the patient’s array of needs…

CBC – a complete blood count test measures the amount of red blood cells (which carry oxygen) and white blood cells (which fight infection); this test gives a good indication of bleeding and infection.
ABGs – an arterial blood gases test measures the acidity (pH) and the levels of oxygen and carbon dioxide in arterial blood; this test determines how well the patient’s lungs are performing gas exchange.
Lactate Level – normal blood lactate levels are 1.3 mmol/L; an increase in lactate production is usually caused by impaired tissue oxygenation whereby the lungs switch from performing aerobic to anaerobic respiration.
Cross Match – this is done in case the patient is found to be needing a blood transfusion.
Electrolytes – electrolyte imbalance can be indicative of shock in the progressive phase.
Clotting – impaired coagulation and microclots are indicative of shock in the progressive phase.
Alcohol Levels – these are tested if the patient suffered from trauma.
ECG – an ECG determines whether the patient is suffering from arrhythmias or is heading towards cardiac depression and failure.
Cardiac Enzymes – cardiac enzymes a.k.a. cardiac biomarkers are released by the heart in the case of heart damage or stress caused by low oxygen; Troponin and creatinine phosphokinase (CPK) levels rise following a heart attack; elevated heart enzyme levels may also indicate acute coronary syndrome or ischaemia.
X-rays, CT scan of the Patient’s Chest, Abdomen and Spine – determines if there is infection, injury, and fluid loss.

Retrieved from https://veteriankey.com/blood-gas-acid-base-analysis-and-electrolyte-abnormalities/ on 16th January 2023

Diagnosis

Clinical manifestations of shock vary according to both the underlying cause and the stage it is at, varying based on the cause of shock as well as the patient’s physiological response.

Typically, a patient is considered to be in shock when the following signs are noted:

a systolic blood pressure of <90mmHg
tachycardia OR bradycardia
altered mental status

Shock Nursing Management

Shock nursing management aims to:

RESTORE ADEQUATE TISSUE PERFUSION – this can be achieved through ensuring adequate oxygen delivery to the cells in relation to gas exchange, cardiac output, and haemoglobin, as well as improving oxygen utilisation by the cells
PREVENT SHOCK PROGRESSION INTO FURTHER STAGES

Thus, in shock nursing management, the following steps need to be tackled as needed:

improving oxygen supply
administering fluid therapy
administering cardiovascular drugs
providing nutritional support
providing psychosocial care

1. Improving Oxygen Supply

With adequate oxygen supply we aim to:

achieve adequate gas exchange – ensure the patient has a patent airway, and improve ventilation and oxygenation by providing supplemental oxygen and mechanical ventilation if required
achieve adequate cardiac output – aim to control the patient’s heart rate, preload and afterload, and cardiac contractility through the administration and titration of fluids and cardiovascular drugs

2. Administering Fluid Therapy

Fluid therapy administration is necessary for all types of shock, though the type of fluid administered and the amount and speed of delivery varies with every patient.

Fluids help increase oxygenation since oxygenation is partly affected by circulation. Types of fluids administered include:

crystalloids – electrolyte solutions such as Isotonic (eg. normal saline or RLactate), Hypertonic (eg. 10% Dextrose) or Hypotonic (eg. 0.45% NaCl – Sodium Chloride)
colloids – types of colloids, which contain large molecules, include blood and its products such as Fresh Frozen Plasma (FFP), as well as synthetic plasma expanders such as Gelafundin (a colloidal plasma volume substitute in an isotonic balanced whole electrolyte solution that can be used for prophylaxis and therapy of hypovolaemia and shock); ADVANTAGES: colloids remain in the intravascular space, restoring fluids faster and with less volume, while blood restores Hgb; DISADVANTAGES: colloids are expensive, may cause reactions, and may also leak out of damaged capillaries, causing additional problems especially within the lungs

fluid administration Complications

Common fluid administration complications include cardiovascular overload and pulmonary oedema.

Patients with increased risk include elderly patients and patients with a history of chronic renal failure or heart failure.

To avoid fluid administration complications, the nurse should:

monitor and document urine output and fluid intake
monitor for changes in the patient’s vital signs
check for lung sounds
perform haemodynamic monitoring

3. Administering Cardiovascular Drugs

Anti-dysrhythmic agents

anti-dysrhythmic agents such as Amiodarone prevent or treat abnormal heart rates and rhythms

Vasodilators

vasodilators such as nitrates cause arterial dilation by decreasing the afterload following decreased resistance to blood ejection, leading to an increase of cardiac output without increased oxygen demands
vasodilators also cause venous dilation by reducing the preload and subsequently reducing the filling pressure on the failing heart

NOTE: Vasodilators REDUCE BLOOD PRESSURE! Monitor patient at all times whilst on vasodilators!

Inotropes and Vasoconstrictors

inotropes and vasoconstrictors increase myocardial contractility leading to an increase in cardiac output
inotropes stimulate adrenergic receptors, causing similar effects to the fight or flight reaction; types of sympathomimetic agents include naturally occurring catecholamines eg. adrenaline, noradrenaline and dopamine; synthetic cathecolamines eg. dobutamine

NOTE: Vasoconstrictors INCREASE BLOOD PRESSURE!

ADRENALINE (EPINEPHRINE)

binds to beta 1 and beta 2 receptors
cause an increase in heart rate, cardiac contractility, vasodilation, and cardiac output
with an increasing rate of infusion also comes an increase in alpha receptors, which result in increased blood pressure and vascular resistance through vasoconstriction
the heart now needs to work harder and so, its oxygen demand increases too

NORADRENALINE

binds to beta 1 receptors only
does not cause an increase in heart rate
a low dose of noradrenaline increases cardiac contractility, leading to an increase in cardiac output
higher doses tend to limit effect due to alpha stimulation which causes massive vasoconstriction
whilst this causes an increase in blood pressure, it compromises peripheral circulation and increases the workload of the heart

DOPAMINE

dopamine is the chemical precursor of noradrenaline
a low dose of dopamine stimulates dopaminergic receptors, causing renal and mesentric vasodilation, leading to a good urine output
a moderate dose of dopamine stimulates beta 1 receptors, causing an increase in cardiac contractility and cardiac output
a high dose of dopamine stimulates alpha receptors, causing massive vasoconstriction, an increase in blood pressure, and an increase in the workload of the heart

DOBUTAMINE

dobutamine causes no dopaminergic effects
dobutamine mainly stimulates beta 1 receptors, causing an increase in cardiac contractility and cardiac output; dobutamine may also stimulate beta 2 receptors, causing mild vasodilation, causing a reduction the the preload, afterload, and stress on the heart
dobutamine is helpful in treating heart failure, especially in hypotensive patients who are unable to tolerate vasodilators
dobutamine may also be used as an adjunct therapy to adrenaline or noradrenaline and dopamine to reduce vasoconstriction effect

ADMINISTRATION OF INOTROPES:

correct dilution of inotropes is of utmost importance
inotropes are administrated as infusions through electronic pumps so that consistent administration is ensured
administration of inotropes is done through a central line
careful haemodynamic monitoring is very important especially since it help in the titrating process of inotropes dosage as needed
inotropes should NOT replace fluid and electrolyte balance
inotropes should be weaned off slowly

EFFECTS OF ADRENERGIC RECEPTORS

RECEPTOR	LOCATION	RESPONSE
ALPHA	skin, muscles, kidneys, and intestines	constrict peripheral arterioles
BETA 1	cardiac tissue	increase heart rate and cardiac contractility
BETA 2	vascular and bronchial smooth muscle	dilates peripheral arterioles; increases heart rate; causes bronchodilation

4. Providing Nutritional Support

Shock causes increased metabolic rates, which in return increase the patient’s energy requirements. Catecholamines (adrenaline and noradrenaline) deplete glycogen stores in 8-10 hours, after which the body starts breaking down skeletal muscle for energy. This prolongs recovery period unless it is prevented.

Typically, a patient in shock may require >3000kcal daily, however, the patient is usually unable to eat due to intubation, sedation, and anxiety. For this reason, enteral or parenteral nutrition should be initiated within 48 hours, and increased to full nutrition by day 3-7, if the patient is haemodynamically stable (excessive nutrient intake should be avoided in the early phase of critical illness).

NOTE: patients diagnosed with shock are also prone to develop pressure ulcers.

5. Providing Psychosocial Care

Psychological care should be provided throughout the whole course of hospitalisation, especially within the critical care environment. Liaise with other healthcare professionals as needed.

Whilst adopting an empathic approach, provide information and reassurance to both the patient (if conscious; if unconscious still talk to your patient as if he/she is listening, making him/her aware of what is going on in relation to care) and relatives, as this reduces anxiety. Communicate with the patient’s relatives about the patient’s condition as well as procedures being performed.

Shock Nursing Management Additional Interventions

ensure good vascular access for fluid administration, central venous pressure (CVP) monitoring, and to draw blood for investigations
insert a NGT (or OGT if patient has facial trauma) so that emesis (vomiting) and aspiration are prevented
insert a urinary catheter to monitor urine output and fluid balance accordingly
monitor the patient’s temperature and ensure maintenance of normal body temperature
reposition patient frequently to prevent pressure ulcer formation
provide frequent mouth and eye care
assess for pain and administer analgesics as needed
ensure continuous monitoring and documentation

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The Definition, Classification and Pathophysiology of Shock

In order to understand how to care for a patient in shock, we must first understand the pathophysiology of shock, as well as how to assess, diagnose, and manage it through appropriate nursing interventions. The most common types of shock are the Hypovolaemic Shock, Cardiogenic Shock, and Septic Shock. Throughout this blogpost we will be looking in detail at the definition, classification, and pathophysiology of shock.

What is Cardiac Output?

Cardiac Output (CO) is the volume of blood ejected from the heart over 1 minute. In adults, normal Cardiac Output is between 4-6L/min.

Cardiac Index (CI) is a haemodynamic parameter related to the cardiac output from the left ventricle in 1 minute to body surface area (BSA). In adults, normal Cardiac Index should be between 2.5-4L/min/m2.

Stroke volume (SV) is the volume of blood pumped out of the left ventricle during each systolic cardiac contraction.

Mean Arterial Pressure (MAP) is the average arterial pressure throughout one cardiac cycle, systole, and diastole.

Systemic Vascular Resistance (SVR) is the resistance in the circulatory system which affects the blood pressure and the flow of blood. SVR is also a component of cardiac function, eg. vasoconstriction leads to an increased SVR.

Formulas:

Cardiac Output (CO) = Heart Rate (HR) X Stroke Volume (SV)

Cardiac Index (CI) = Cardiac Output (CO) / Body Surface Area

Mean Arterial Pressure (MAP) = Cardiac Output X Systemic Vascular Resistance (SVR)

Cardiac Output Determinants

HEART RATE – influenced by both the sympathetic and parasympathetic system, as well as by intrinsic regulation
STROKE VOLUME – determined by cardiac preload (PL), afterload (AL), and cardiac contractility (CC).

Preload determinants

Preload (PL) is the stretching force exerted on the ventricle by the blood contained within at the end of diastole.

The Starling’s Law of the Heart indicates that increased volume returned to the heart causes an increase in Cardiac Output, however, following a certain increase in volume returned causes a decrease in Cardiac Output.

Retrieved from https://ecgwaves.com/topic/pressure-volume-curves-preload-afterload-stroke-volume-wall-stress-frank-starlings-law/ on 10th January 2023

Preload determinants include:

VOLUME OF BLOOD RETURNED TO LEFT VENTRICLE – influenced by venous return, total blood volume, and atrial kick
LEFT VENTRICLE COMPLIANCE (stretching ability) – influenced by the stiffness and thickness of the muscle wall

Examples: in Hypervolaemia, preload is too low, whilst in Congestive Heart Failure, preload is too much.

Afterload Determinants

Afterload (AL) is the resistance (a.k.a. Systemic Vascular Resistance SVR) that the heart must overcome to push blood into the systemic circulation.

An increase in Afterload causes an increase in the required effort and oxygen demand by the heart, eg. vasoconstriction increases Systemic Vascular Resistance, total blood volume and viscosity.

To reduce the heart’s workload we can provide therapeutic nursing management, including the administration of vasodilators.

pathophysiology of shock — Retrieved from https://www.studypk.com/articles/nursing-mnemonics-preload-vs-afterload/ on 10th January 2023

Cardiac Contractility Determinants

Cardiac Contractility (CC) is the force by which the heart contracts. CC is determined by:

VENOUS RETURN – Starling’s Mechanism
- STIMULATION OF THE SYMPATHETIC NERVOUS SYSTEM
- INCREASE IN INTRACELLULAR CALCIUM (Ca++) – such as after use of Digoxin
- PHARMACOLOGICAL INTERVENTIONS – eg. administration of Inotropes

Retrieved from https://step1.medbullets.com/cardiovascular/108003/cardiac-output-and-variables on 11th January 2023

Shock Definition

Shock can be defined as an acute widespread process of impaired tissue perfusion resulting in cellular, metabolic and haemodynamic changes, causing an imbalance between cellular oxygen supply and demand. Shock leads to death if not controlled in time.

Normal tissue perfusion requires:

adequate blood volume
adequate cardiac pump
effective circulatory system

Impairment of any of the above, thus, impairment in normal tissue perfusion, may lead to SHOCK…

Impaired oxygen perfusion causes:

inadequate blood flow reaching the tissues
inadequate delivery of oxygen and nutrients to the cells
cell starvation due to oxygen and nutrient deprivation
cell death
multiple organ failure
death

Classification of Shock

Shock can be classified into 3 different types. Whilst the management of shock varies based on the type of shock it is, the resulting effect of all 3 types of shock is the same – decreased tissue perfusion.

Hypovolaemic Shock

Hypovolaemic shock is the most commonly occurring type of shock, which is also easily reversible if treated in a timely manner. Features of a hypovolaemic shock include:

loss of circulating or intravascular volume
impaired tissue perfusion
inadequate delivery of oxygen and nutrients
may be caused by relative and absolute hypovolaemia, or loss of blood or other fluids

Retrieved from https://twitter.com/misirg1/status/1382458804995035144 on 19th January 2023

Cardiogenic Shock

impaired ability of the heart to pump blood as it should (left or right ventricle dysfunction), causing systemic hypoperfusion and tissue hypoxia
may be caused by cardiac injury (eg. cardiac tamponade), cardiopulmonary arrest, following cardiac surgery, dysrhythmias (severe tachycardia or bradycardia), myocardial tissue necrosis following a Myocardial Infarction, or structural problems (eg. valvular damage or regurgitation, pulmonary embolus, acute myocarditis, papillary muscle rupture, intracardiac tumour, and congenital defects
compensatory mechanisms may worsen the situation…eg. reduced cardiac output due to myocardium death causes increased contractility which further increases the heart’s workload and oxygen demand; reduced blood pressure causes the release of catecholamines which leads to vasoconstriction, subsequently leading to a further increase in cardiac workload and oxygen demand

Retrieved from https://www.facebook.com/jamajournal/photos/a.10158814898548341/10158814906348341/?type=3&locale=zh_HK on 19th January 2023

Distributive Shock

impaired distribution of circulating blood volume
vasodilation
capillary leaks

Distributive Shock is further sub-classified into 3 other types of shock:

SEPTIC SHOCK:

microorganism entry into the patient’s body
dysregulated host response characterised by excessive peripheral vasodilation, causing maldistribution of blood volume, over-perfused peripheral areas and under-perfused central areas
is the major cause of admission in the critical care setting

Septic Shock may originate from the community (>80% of cases) or during a stay in a healthcare facility.

ANAPHYLACTIC SHOCK:

severe antigen-antibody reaction causing histamine release
signs & symptoms include vasodilation, hypotension, bradycardia, increased capillary permeability, bronchospasm, laryngeal oedema, and stridor

NEUROGENIC SHOCK:

disruption of sympathetic nerve activity below the level of a spinal cord injury or disease
signs & symptoms include vasodilation, hypotension, bradycardia, warm dry skin, and loss of thermoregulation

Obstructive Shock

obstructive shock is often classified with cardiogenic shock
obstructive shock is mechanical obstruction which impedes the heart from generating adequate cardiac output
examples of obstructive shock include Tension Pneumothorax, Pericardial Tamponade and Pulmonary Embolus

The Pathophysiology of Shock

Initial Stage

Within the initial phase of shock, effects are very subtle and at cellular level. An increase in serum lactate indicates metabolic acidosis due to cells switching from aerobic to anaerobic respiration.

Decrease in Cardiac Output
Decrease in tissue perfusion
Cells switch from aerobic to anaerobic respiration
Accumulation of Lactic Acid
Lactic Acidaemia (Low pH)
Cellular Damage

Compensatory Stage

During the compensatory stage of shock, the patient’s body attempts to improve tissue perfusion through neural, chemical, and hormonal compensation, mediated by the sympathetic nervous system.

NEURAL COMPENSATORY MECHANISMS

increased Heart Rate and Cardiac Contractility
arterial and venous vasoconstriction
circulation lessens within the peripheries and becomes more focused on vital organs perfusion

CHEMICAL COMPENSATORY MECHANISM

chemoreceptors detect acidosis and stimulate hyperventilation so more Carbon Dioxide is exhaled

HORMONAL COMPENSATORY MECHANISMS

Hormonal compensatory mechanisms aim to increase the blood pressure to cause an increase in tissue perfusion.

the anterior pituitary gland is stimulated, causing secretion of ACTH (Adrenocorticotropic Hormone), which then stimulates the adrenal cortex to produce glucocorticoids (glucagon), which causes an increase in blood glucose level
the adrenal medulla is also stimulated, causing the release of adrenaline and noradrenaline, which result in vasoconstriction, leading to an increased Blood Pressure and increased Heart Rate
renin response is activated, which facilitates the conversion of Angiotensinogen into Angiotensin II; this conversion causes vasoconstriction, release of aldosterone (which leads to sodium retension), and release of antidiuretic hormone (ADH) by the posterior pituitary gland (which leads to water retention)

SYMPTOMS EXPERIENCED DURING THE COMPENSATORY PHASE:

cold, clammy skin
drop in urine output
tachycardia
tachypnoea
hyperglycaemia

Progressive Stage

compensatory mechanisms start failing
shock cycle continues indefinitely
anaerobic respiration causes energy exertion within the cells
cells are unable to function, and irreversible damage occurs (Mitochondria become unable to use oxygen for the production of energy, and Lysosomes release digestive enzymes which then cause further cellular damage)
utilisation of the limited oxygen delivered into the cells becomes problematic

During the progressive stage, organ systems start to fail…

Myocardial Hypoperfusion causes decreased Cardiac Output leading to ventricular failure, enabling shock to progress further
Decreased Cerebral Blood Flow causes CNS dysfunction, causing failure of the sympathetic nervous system, failure of the thermoregulation mechanism, cardiac and respiratory depression, and altered mental status
Impaired Coagulation leading to microclot formation, which may cause Disseminated Intravascular Coagulation (DIC)
Renal Vasoconstriction & Hypoperfusion causes decreased urine output and increased creatinine, which may also lead to Acute Tubular Necrosis (ATN)
GastroIntestinal Tract Hypoperfusion causes decreased peristalsis (decreased bowel sounds), release of Gram-negative bacteria (which worsens shock), and liver hypoperfusion due to deranged LFTs
Pulmonary Vasoconstriction along with microemboli, parenchymal inflammation, and alveolar oedema all lead to respiratory failure (Acute respiratory distress syndrome ARDS)

SYMPTOMS EXPERIENCED DURING THE PROGRESSIVE PHASE:

electrolyte imbalance
metabolic acidosis
respiratory acidosis
peripheral oedema
tachycardia
arrhythmias
hypotension
pallor
cool clammy skin
altered level of consciousness
reduced bowel sounds

Refractory Stage

In the final stage of shock, the patient becomes unresponsive to treatment, experiences multiple organ failure, eventually leading to death.

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Preventing Secondary Brain Injury

Primary brain injury can only be prevented through education and health promotion, and surviving the initial head injury is only a small part of the battle for the patient with a brain injury. Preventing secondary brain injury is even more important since it may have a greater influence on the final outcome than the primary brain injury itself. Throughout this blogpost we will go through ways of preventing secondary brain injury as much as possible.

Causes of Secondary Brain Injury

Causes of secondary brain injury include:

hypoxia
hypotension
hypercapnia
acidaemia
anaemia
intracranial mass
hyperglycaemia OR hypoglycaemia
hyperthermia OR hypothermia

Preventing secondary brain injury is possible by preventing ALL mentioned causes through early treatment
Most causes mentioned are related to raised ICP – Intracranial Pressure

The Monro-Kellie Hypothesis

The Monro-Kellie hypothesis states that the total volumes of brain (approximately 80%), CSF (approximately 10%) and intracerebral blood (approximately 10%) are constant. The cavity in which these three are housed a.k.a. the cranial cavity, is not able to expand, and so, an increase in one should cause a decrease in one or both of the remaining two. This ensures that the total volume of the three components remains fixed, and that no rise in ICP is caused.

ICP (Intracranial Pressure) is the pressure exerted by the intracranial contents against the skull. The brain normally is able to tolerate a significant increase in intracranial volume WITHOUT increasing much the ICP. If, however, this normal compensation mechanism becomes exhausted and the compliance limit is exceeded, an increase in ICP becomes imminent.

NOTE: an increase in ICP causes changes within the patient’s Vital Signs.

In normal circumstances, ICP is less than 10mmHg (in adults). If ICP increases to >20mmHg treatment is required!

preventing secondary brain injury — Retrieved from https://resources.wfsahq.org/atotw/cerebral-physiology-part-2-intracranial-pressure-anaesthesia-tutorial-of-the-week-71/ on 2nd January 2023

Signs of Increased ICP

unexplained changes in vital signs
cushing’s triad – isolated systolic hypertension, bradycardia, and altered breathing patterns
headache
nausea & vomiting
sensory deficits
impaired motor function
pupillary changes – if ICP >18mmHg
altered level of consciousness
decreased level of consciousness
seizures

Cushing’s Triad

Monitoring Intracranial Pressure

Monitoring ICP can be done through the use of:

ventriculostomy – intraventricular catheter
subarachnoid bolt or screw
subdural OR epidural catheter or sensor
fibreoptic transducer-tipped intraparenchymal catheter
non-invasive methods such as an automated IR pupillometry

Possible Causes of Increased ICP

Pathological Causes	Non-Pathological Causes
traumatic brain injury	coughing / sneezing
temperature	lifting / bending / body positioning
intra-thoracic pressure	stress / emotional responses
intra-abdominal pressure	pain
acidosis / hypoxia	blood pressure changes
lesions occupying space eg. bleeding, hydrocephalus, tumour, oedema, abscess, infection	valsalva manoeuvre

Factors affecting ICP

MAP : Mean Arterial Pressure – both hypertension and hypotension may raise ICP
Brain Trauma – expanding lesions increase ICP and may cause herniation a.k.a. brain matter displacement
CMR Changes – Changes in Cerebral Metabolic Rate may happen due to hyperthermia and increase in blood flow to meet demands, which leads to an increase in ICP
Conditions Causing Acidosis – results in cerebral vascular dilation such as hypoxia, ischaemia, and hypercapnia
Increased Intra-Thoracic / Intra-Abdominal Pressure – may happen during coughing or suctioning and due to high PEEP
Conditions Affecting Venous Return – pressure on jugular veins or patient positioning

Cerebral Perfusion Pressure

Cerebral Perfusion Pressure CPP is the difference between the MAP (Mean Arterial Pressure) and the ICP.

CPP = MAP – ICP

Ideally, CPP should be between 50-70mmHg, as this ensures an adequate blood supply to the brain. On the other hand, ICP should be approximately 10mmHg.

A decrease in CPP or rise in ICP may cause ischaemia, neuronal hypoxia, and even death.

NOTE: if MAP = ICP, cerebral blood flow may cease.

Preventing Rise in Intracranial Pressure

1. Control of Vital Signs

HYPOTENSION reduces oxygen and nutrient perfusion; CPP = MAP – ICP; aim for MAP of >80mmHg to ensure CPP of >60mmHg with ICP of 20mmHg; to increase blood pressure administer fluids and vasopressors.
HYPERTENSION may result following interventions or due to decreased cerebral perfusion; sedatives may help avoid blood pressure from increasing during procedures; primary anti-hypertensives such as beta blockers can be administered, but only if ICP is monitored, OR SBP is >180mmHg, OR MAP is >110mmHg; AVOID vasodilators as these increase ICP.

2. Ventilation

HYPERCAPNIA causes vasodilation – a 30% increase in cerebral blood flow leads to a 10mmHg increase in PaCO2, which raises ICP.
HYPOCAPNIA causes vasoconstriction, which in return reduces cerebral blood volume and ICP, leading to ischaemia.
HYPOXIA causes cerebral vasodilation, leading to an increased intracranial blood volume and increased ICP (high levels of PaO2 have not shown evidence of any affect on CBF).
GOOD OXYGENATION should be maintained (ideal SPO2 of >95% and PaO2 of >80mmHg), if needed, through intubation and mechanical ventilation. IMPORTANT – avoid high tidal volume (as this may cause acute lung injury) and use a low level of PEEP (5-8mmHg) to maintain good oxygenation.
pH BALANCE should be maintained between 7.35 and 7.45
AIM FOR LOW NORMAL PaCO2 (approx. 35mmHg) – although hyperventilation may be required temporarily to reduce cerebral vasodilation and enhance venous return; AVOID LOW PaCO2 as excessive vasoconstriction leads to ischaemia, restricting oxygen supply to the injured area, leading to an increase in damage.

Relationship between CBF and PaC02 (1st image) & Relationship between CBF and PaO 2 showing almost no effect on CBF in the
normoxaemic range (2nd image); CBF increases if PaO 2 is less than 50mmHg. – Retrieved from https://www.frca.co.uk/Documents/170907%20Cerebral%20physiology%20I.pdf on 3rd January 2023

3. Patient Positioning

ELEVATE HEAD OF BED to about 30% – patient’s neck should be3 kept midline; gravity promotes CSF and venous drainage, resulting in a lowered ICP; NOTE: evidence as to whether or not bed elevation may lower CPP has been inconclusive in a recent systematic review (Alarcon et al., 2017).
VENOUS RETURN OBSTRUCTION causes an increased ICP due to factors such as head rotation to one side, extreme flexion of arms and hips, neck angulation and pressure on jugular veins (eg. from tight ETT tie or lateral positioning), trendelburg positioning, and prone positioning.

4. Procedures & Environmental Factors

SUCTIONING
RAPID POSITION CHANGES
PAIN & COUGHING
VENEPUNCTURE
REMOVING ADHESIVE TAPE
USE OF BEDPANS/ENEMA

AVOID ACTIVITY CLUSTERING and instead promote resting periods between procedures mentioned above. If needed, a short acting sedative may be administered as a bolus prior to the procedure.
AVOID UNNECESSARY INSTRUMENTAL TOUCH & PAINFUL PROCEDURES
REDUCE LIGHTING in the patient’s room
REDUCE UNNECESSARY ENVIRONMENTAL NOISE such as unneeded alarms – set appropriately and in relation to the patient’s norms
SUCTIONING increases intra-thoracic pressure, impedes venous return and increases ICP; hypoxia may lead to cerebral ischaemia. Reduce impact on the patient by providing hyperoxygenation before and/or after the procedure, hyperventilating, suctioning using a closed suction system, limiting the frequency and the duration of suctioning, administering a sedation bolus, or Lignocaine IV or via Tracheal Tube.

NOTE: Some studies have shown that the presence, touch, and voice of patient relatives may help decrease ICP. Other unrelated studies have also shown that oral hygiene, bed bathing, catheter care and chest percussion do not result in a significant rise in ICP.

Retrieved from http://www.learnpicu.com/neurology/ICP (left image) & http://pedsccm.org/FILE-CABINET/head_trauma/sld028.htm (right image) on 3rd January 2023

5. Sedation & Analgesia

SEDATIVES, MUSCLE RELAXANTS & ANALGESICS can help reduce the effects of unpleasant procedures; Sedatives administered are usually opioids or benzodiazepines; Muscle relaxants should be avoided if possible, and should they be administered, ensure that the patient is sedated first.
ADEQUATE VENTILATION may also be achieved through the effect of sedation and analgesia.
ATTENTION!! Sedation and Analgesia may affect the MAP, leading to an affect on the CPP (cerebral perfusion pressure), thus, ensure adequate fluid volume. Similarly, sedation and analgesia may also mask certain aspects related to the neuro assessment, thus, for a patient on such medication, rely more on pupillary reaction rather than the neuro assessment.

6. Fluid Management

In relation to OSMOTIC THERAPY, large molecules (eg. Mannitol) or Hyperosmolar solution (eg. hypertonic saline, which is considered to be superior and with less side effects) remain in circulation, increasing osmolarity. For osmosis to happen, an intact blood-brain-barrier is required, where fluid is drawn from diluted areas to more concentrated areas (from extracellular to intravascular space). This reduces cerebral oedema whilst improving blood flow.
When administering osmotic therapy, CAREFUL MONITORING is required – monitor electrolyte levels especially Potassium and Sodium; replace fluid as necessary to avoid hypovolaemia; serum osmolarity should not exceed 320mOsm/L…higher levels may induce pulmonary oedema or rebound cerebral oedema.
HYPERTHERMIA, unless infection is involved, may be induced by localised damage in the thermoregulatory centre within the hypothalamus. A 1°C rise in body temperature causes 6-10% increase in cerebral metabolic rate, increased oxygen demand, increased blood flow and volume due to vasodilation, and increased ICP. IMPORTANT: monitor the patient’s body temperature and help cooling by removing any extra blankets and administering antipyretics.
THERAPEUTIC HYPOTHERMIA may reduce ICP, however, evidence of improved survival is still inconclusive to date. Additionally, avoid rapid cooling as shivering raises ICP, thus, should be prevented.

7. Seizure Control

POST-TRAUMATIC SEIZURES happen in 5% of patients with head injuries.
Seizures increase CEREBRAL METABOLIC DEMANDS: increased blood flow causes an increase in ICP; if flow doesn’t meet the cerebral metabolic demands, the patient experiences ischaemia and neuronal destruction.
PHENYTOIN is considered to be an effective medication in the prevention of early seizures (always monitor serum levels when administering).

8. Nutrition & Elimination

PROTEIN is very much required by a hypermetabolic brain.
STRESS ULCER PROPHYLAXIS is commonly administered to patients with an increased risk of stress-related mucosal bleeding from the upper gastrointestinal tract. Apart from administering early enteral feeding, ideally through an orogastric tube, administer pharmacological prophylaxis such as H2-blockers, proton-pump inhibitors, or sucralfate.
Attempt to maintain NORMOGLYCAEMIA – hyperglycaemia is associated with increased ICP, while hypoglycaemia is associated with aggravated brain injury. It’s also important to mention that intensive insulin therapy does not improve outcome, and may actually worsen the patient’s condition and prognosis.
STOOL SOFTENERS may be required especially if the patient is constipated, since constipation increases intra-abdominal pressure and ICP.
GASTRIC DECOMPRESSION is intended for patientS with gastric distention receiving aggressive ventilatory resuscitative measures prior to intubation. A NG tube may be used to perform gastric decompression for the patient with known or suspected gastric distension. Check tube placement. Attach suction or a large syringe and evacuate the stomach.NOTE: for patients with facial trauma use an orogastric tube instead.

In Summary…

List of Interventions to Minimise ICP

1. AIRWAY & VENTILATION

monitor pH, pCO2 and pO2
if GCS <9 ensure early intubation and mechanical ventilation
avoid tight ETT or Tracheostomy ties
avoid high PEEP
suction only when necessary
keep head elevated and aligned
provide mouth care to eliminate oral secretions
perform gastric decompression

2. ICP & CPP

prevent rise in ICP
prevent drop in CPP
remember: CPP = MAP – ICP
mannitol or furosemide may be administrated to reduce intracellular volume
hypertonic saline reduces cerebral oedema whilst improving blood flow

3. NEUROLOGICAL & HAEMODYNAMIC MONITORING

avoid drops in the patient’s blood pressure
monitor the patient neurological status through the Glasgow Coma Scale and Pupil Reactivity

4. NUTRITION & FLUIDS

ensure adequate nutrition and fluid intake as indicated
fluid restriction may be indicated so as to prevent an increase in ICP
monitor the patient’s electrolytes
an adequate MAP can be achieved through administration of normal saline +/- inotropes
monitor for diabetes insipidus (a rare condition which causes increased urination (polyuria) and increased thirst (polydipsia); Diabetes Insipidus is not related to type 1 or type 2 diabetes)

5. PREVENTION

prevent hyperthermia
prevent hyperglycaemia
prevent hypoglycaemia
prevent seizures
prevent pain
prevent anxiety
prevent venous thromboembolism VTE

6. NEUROLOGICAL INTERVENTIONS

an expanding haematoma may require ventriculostomy for CSF drainage and ICP monitoring
craniectomy may also be indicated if an increase in space is required

7. PATIENT SAFETY

ensure patient safety at all times

8. PSYCHOSOCIAL CARE

promote congnitive function
provide support to the patient’s relatives
provide health literacy and rehabilitation advice to the patient and relatives

References

Alarcon, J. D., Rubiano, A. M., Okonkwo, D. O., Alarcón, J., Martinez-Zapata, M. J., Urrútia, G., & Bonfill Cosp, X. (2017). Elevation of the head during intensive care management in people with severe traumatic brain injury. The Cochrane database of systematic reviews, 12(12), CD009986. https://doi.org/10.1002/14651858.CD009986.pub2

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Performing a Neurological Assessment – GCS & Pupillary Reaction

Performing a Neurological Assessment

When performing a neurological assessment, one would be assessing the nervous system for the purpose of identifying abnormalities affecting the activities of daily living. The Glasgow Coma Scale (GCS) is an assessment tool which can objectively describe the extent of consciousness impairment incurred by acute medical and trauma patients. Similarly, pupillary reaction is assessed as an attempt to trigger a normal physiological response to the size of the pupil via the optic and oculomotor cranial nerve.

The Glasgow Coma Scale GCS Neurological Assessment

Through the use of the Glasgow Coma Scale GCS the nurse assesses the patient’s level of consciousness in a way that determines the degree of stimulation required to elicit a response.

the GCS is based on 3 modes of behaviour, namely Eye Opening, Verbal Response, and Motor Response
the GCS’s overall score should not be used alone in determining clinical findings, and must be combined with Pupillary Reaction and Vital Signs
the patient can score from 3 to 15, with 15 being the best score possible, and 3 being the least score possible; a patient with a score of <9 is considered to be severe, requiring an ETT
repeated observations indicate static, improving, or worsening of the patient’s neurological condition
action must be taken even if minor changes are noted

Retrieved from https://www.firstaidforfree.com/glasgow-coma-scale-gcs-first-aiders/ on 29th December 2022

neurological assessment — Retrieved from https://standardofcare.com/abnormal-posturing/ on 29th December 2022

Structured GCS Assessment

#1 – CHECK

identify factors which may interfere with assessment such as pre-existing factors (eg. language barrier, intellectual deficits), effects of current treatment (eg. sedation or tracheostomy), and effects of pre-incurred injuries (eg. cranial fracture or spinal cord damage)
if any of the above factors are determined, NT (Not Testable) should be recorded, and no total score should be listed

#2 – OBSERVE

observe patient for evidence of spontaneous behaviour
if no spontaneous behaviour is noted, observe behaviour in response to stimulation

#3 – STIMULATE

try to illicit a response by increasing the stimulus intensity gradually
for auditory stimulus, speak, and if needed, shout, using the patient’s preferred name
for physical stimulus to illicit eye opening, use a peripheral method by pressing on the distal part of the patient’s fingernail, increasing the intensity for up to 10 seconds
for physical stimulus to illicit localisation, use central methods such as the trapezius pinch or the supra-orbital notch pressure
AVOID sternal rub since this method can cause bruising to the patient!

#4 – RATE

if during your initial ‘check’ you determine that certain domains are not testable, document as NT and do not list total score
determine if top criteria is met based on observation – if yes, document appropriately; if no, attempt to illicit a response through stimulus as mentioned above
in relation to motor response, different responses between the left and right side (arms or legs) of the patient, document the best response
different responses between the peripheral stimulus and central stimulus, document the response stimulated centrally

NOTE:

EYE OPENING aim is to assess brain stem function
VERBAL RESPONSE aim is to assess interpretative speech and language area in the temporal lobe within the brain
MOTOR RESPONSE aim is to ascertain whether the cerebral cortex can interpret sensory messages and translate them to a motor response

Retrieved from https://www.physio-pedia.com/Glasgow_Coma_Scale on 29th December 2022

For more information about the Glasgow Coma Scale please visit https://www.glasgowcomascale.org/

Pupillary Reaction

In the Critical Care setting, the eyes are considered to be a ‘window to the brain’.

pupillary reaction to light may be brisk, sluggish, or fixed
sluggish, suddenly dilating, or unequal pupils may indicate compression of oculomotor cranial nerve (3rd), and/or compressed brain stem due to oedema or haematoma worsening; urgent intervention may improve outcome
pinpoint pupils may indicate narcotic/opioid use

NOTE: certain eye drops such as Atropine may dilate pupils.

Additional Signs & Symptoms

Autonomic Dysfunction a.k.a. Dysautonomia – happens when the autonomic nervous system, which controls functions responsible for wellbeing and maintaining balance, does not regulate properly; signs include hypertension and hyperpyrexia
Persistent Vegetative State – a state of ‘eyes-open unresponsiveness’ in patients in a coma for 30 days or more; it is considered to be a chronic disorder in which a patient with severe brain damage appears to be awake but shows no evidence of awareness of their surroundings
Prolonged Unconsciousness a.k.a. Coma – a prolonged state of unconsciousness during which a person is unresponsive to their surrounding environment; while the patient is alive and looks like they are sleeping, they cannot be awakened by any stimulation, including pain

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