Septic Acute Kidney Injury – More than just Hypo Perfusion


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imageSeptic acute kidney injury (SAKI) has long been thought to be characterised by hypo perfusion (decreased blood flow to the kidney) and haemodynamic instability.

Prevention and treatment has been focused on ensuring patients were hemodynamically optimised and stable.

Recent studies have identified that not all patients with SAKI have evidence of hypo perfusion. A complex pathophysiological cascade of events and changes are now beginning to be researched further to gain better understanding of the underlying mechanisms at play


Sepsis (bacteraemia) occurs in response to an infection. Chemicals are released in the body to fight the infection. This triggers a cascade of inflammatory changes which can lead to multi organ damage and failure. Sepsis is potentially life threatening.

Acute Kidney Injury (AKI)

AKI is a syndrome and not a disease – a sudden occurrence of damage to the kidney or kidney failure. The ability of the kidney to filtrate out waste products from the circulatory system is effected causing a build-up of these waste products.

Patients who experience AKI have an increased risk for other health problems ie kidney disease, stroke, heart disease and of further episodes of AKI. Each additional episode of AKI increases the chances of developing Kidney Failure and Kidney Disease.

Until recently it was believed that a major characteristic of SAKI was kidney hypo perfusion.

Studies are now finding that AKI does occur in septic patients without kidney hypo perfusion or haemodynamic deterioration suggesting other mechanisms are at work.

Pathophysiological mechanisms underlying the development and progression of SAKI are quite complex and still not completely understood. Recent studies suggest

“key pathophysiological processes include renal macro circulatory and micro circulatory disturbance, glycocalyx disruption, surge of inflammatory markers and oxidative stress, coagulation cascade activation, imbalanced energy metabolism with release of ATP from damaged cells, bioenergetics adaptive response with controlled cell-cycle arrest, renalvenous congestion, and maladaptive TGF mechanism”


Damage to kidney tissue activates a repair process following the common ischemic reperfusion pathway.

Possibly due to a maladaptive response during this repair process AKI survivors are at a higher risk of Chronic Kidney Disease (CKD) and cardiovascular morbidities and mortality. Each subsequent episode of AKI further increases these risks.

Current treatments for SAKI are supportive therapies by nature

  • Fluid Therapy – use of isotonic crystalloids as initial management for expansion of intravascular volume.
  • Haemodynamic Optimisation – use of fluids and vasopressors help minimise further extension of kidney injury and facilitates renal recovery.
  • Diuretics – with AKI there is an increased risk for fluid overload and therefore use of diuretics is necessary to help rid the body of excess fluid and salt through urine.
  • Renal Replacement Therapy (RRT) – haemodialysis is this use of a dialyser which aides in removing waste from blood, restores electrolyte balance and removes extra fluid from the body.

There are now new and proposed treatments available which target the underlying complex pathophysiological changes of SAKI which are just starting to be used with some confidence.

  • Alkaline Phosphatase (AP) – an endogenous enzyme which has detoxification capacity
  • a-Melanocyte-Stimulating Hormone (a-MSH) – a strong anti-inflammatory cytokine which decreases inflammatory cytokines.
  • Toll-like Receptor 4 Inhibitor (TLR4) – Lipopolysaccharide binds to TLR4 on antigen-presenting cells to inhibit an inflammatory response
  • Heparin – suppresses the activation of inflammatory cells by binding and neutralising inflammatory mediators/enzymes released during the inflammatory phase.
  • Mesenchymal Stem Cells – have a renoprotective effect derived from the paracrine/endocrine secretion of bioactive factors and exosomes.


SAKI is on the rise in many counties possibly due to various factors associated with microorganism resistance to antibiotics, increased use of cytotoxic drugs leading to large numbers of individuals in communities who are immune compromised and an aging population.

Further research and better understanding of the pathophysiology underlying SAKI will provide an opportunity for a more robust and vigorous response by health clinicians to this scenario.

Managing Increased Fluid Loss from Stomas Post Operatively


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The incidence of stoma formation (colostomy, ileostomy, jejunostomy) in the western world for the adult population is 2-4 per 1000 population with colorectal cancer being the most common (65%) indicator for this procedure.

30 % patients with a new stoma experience high output (HOS) defined as more than 1500 ml output in 24 hours on two consecutive days. In the first couple of days post stoma formation output is expected to be somewhat high due to the bowel adapting to the new changes, however, this situation resolves rapidly. Output exceeding 3000 ml in 24 hrs is classed as excessive output stoma (EOS).

Causes of high output from a stoma are

  • Infection 43%stoma-nurseconvo
  • Prokinetic agents (drugs) 14%
  • Unknown 43%

HOS is classified even further as early onset (EHOS) and late onset (LHOS).

Early High Output Stoma

16% stoma patient experience early high output stoma (EHOS) on average occurring around Day 8 post-operatively. EHOS is defined clinically as more than 1500ml per 24 hours on at least two consecutive days within three weeks of stoma formation usually occurring before discharge from hospital.

Late High Output Stoma

The prevalence of late high output stoma (LHOS) is 14% occurring on average around Day 25. The development of HOS occurring more than three weeks post stoma formation is classed as LHOS.

Unfortunately, studies have found that as many as 28% of stoma patients are readmitted to hospital with significant weight loss (5-7 kgs).

23-43% of these readmissions are due to HOS with evidence of electrolyte imbalance and dehydration. Electrolyte imbalance is of significant concern. Magnesium, Potassium and Calcium are particularly affected in this clinical scenario.

Electrolyte Imbalances                                                                     

  • Hypomagnesaemia – low levels of Magnesium is common in stoma patients due to the decrblood-test-nurseconvoeased absorption surface area of the bowel. Magnesium is a key component of many chemical reactions inside the cells of the body which are required for muscle and nerve activity, maintenance of normal heart beat and a healthy immune system.
  • Hypokalaemia – low potassium levels are also common however treatment is less than effective until Magnesium levels are normalised first. Early signs of hypokalaemia are general weakness, muscle cramps and numbness and tingling usually experienced in the lower extremities first.
  • Hypocalcaemia – As per above, treatment for low calcium is less than effective until the Magnesium levels are within normal range.


The first line of treatment for stomas with high output is to diagnose and treat the underlying cause before commencing nutritional and pharmacological intervention.

Clostridium Difficile is seen in an increasing number of hospitalised patients experiencing diarrhoea and HOS patients should be screened to rule out this as a cause of their high stoma output.  Studies suggest this agent is associated with 3-10 per 1000 general hospitalisations.

Medications which have been found to increase the risk for high output are as per below, and consideration should be given to ceasing and or replace with alternative drugs.

  • Metformin
  • Prokinetic (maxalon, laxatives, erythromycin)
  • Cortico-steroid abrupt withdrawal

Bowel Obstruction is another quite serious possible cause for high outputs as is Short Gut Syndrome (intestines fail to absorb enough nutrition and or fluids in and occurs in normal length bowel or shorter bowel due to surgery).

Suggested protocol by Arenas Villafranca et al. describes a 3 stage approach to the treatment of stomas with high output.

Initial treatment includes

  • restricting oral fluid intake to 500-1000 ml per day avoiding hypotonic fluids i.e., tea, coffee, alcohol, fruit juices
  • administering IV replacement therapy
  • prescribing of Loperamide 2mgs before each meal and at night is recommended
  • daily weighs and strict fluid balance and
  • monitoring of blood analysis is necessary and treat imbalances as necessary.

If stoma output has resolved in 2-3 days then increase oral fluid intake, withdraw medication and start serum therapy (injection of serum containing antibodies to the disease specifically being treated)

If high output continues Stage II treatment recommendation is to

  • continue with restricting oral fluidshydration-therapy-nurseconvo
  • increase Loperamide and commence omeprazole
  • If fats, pus or undigested food/medications are present suggestive of malabsorption, steatorrhea or pruritic bilious output add cholestyramine to the medication regime

If the high output persists, a further 2-3 day’s – Stage III is initiated. Stage III includes

  • supplementation with hydro and lipid soluble oral vitamins
  • maintain loperamide
  • add codeine (only if >15ml/min creatinine clearance)
  • increase cholestyramine if malabsorption continues
  • after two weeks if HOS >2000mls add octreotide for 3-5 days if no improvement suspend this treatment.

A success rate of 100% was achieved in Arenas Villafranca et al. study with use of the early examination and treatment protocol as described above.

Given such results consideration for a standardised protocol for the treatment and management of high output stomas, should be formalised.


Primary Reference

Jose J Arenas Villafranca, Cristobal López-Rodríguez, Jimena Abilés, Robin Rivera, Norberto Gándara Adán and Pilar Utrilla Navarro 2015 Protocol for the detection and nutritional management of high-output stomas Nutrition Journal  14:45 DOI 10.1186/s12937-015-0034-z

Additional Reference

Kwiatt M,  Kawata M, 2013, Avoidance and Management of Stomal Complications, Clin Colon Rectal Surg 2013;26:112–121. DOI 10.1055/s-0033-1348050. ISSN 1531-0043.

Rostami K, Al Dulaimi D. 2015 Elemental diets role in treatment of High ileostomy output and other gastrointestinal disorders,  Gastroenterol Hepatol Bed Bench 2015;8(1):71-76).

Risk of phosphate neuropathy from phosphate based enema use


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Use of hypertonic sodium phosphate enemas (ie Fleet) in the elderly may cause severe phosphate neuropathy and  hyperphosphatemia.

Deposits of phosphate crystals form within the kidneys causing kidney dysfunction. Sodium phosphate is absorbed into the blood stream due to the significant absorption properties found in the bowel.

Cleansing enemas are used in hospitals for pre operative bowel preparation and when bowel activity has not occurred for many days and the risk of bowel obstruction is real. First line treatment should always be non pharmacological. In addition to strategies below patients should be provided with opportunities to sit on a toilet/commode regularly (at least daily particularly postprandially).

  • patient education                             image
  • hydration
  • diet
  • activity

Enemas distend the bowel stimulating colon contractibility causing stool expulsion. Phosphate enemas additionally stimulate the bowel muscles to contract facilitating stool expulsion. Adverse effects for all enemas irrespective of the active ingredient includes electrolyte imbalance (metabolic derangement) and bowel perforation.

Bowel perforation can generally be related to muscle weakness of the bowel wall, an obstruction or incorrect positioning of the patient during enema administration. Bowel perforation, hyperphosphatemia and phosphate neuropathy may occur, causing death in up to 4% of cases post enema administration.

Symptoms of acute phosphate nephropathy are:

  • lethagy
  • drowsiness
  • decreased urination
  • swelling of ankles, feet and legs.

Symptoms of hyperphosphatemia potentially are:

  • muscle cramps                                               image
  • joint pain
  • tingling and numbness

and in prolonged states:

  • itchy skin
  • pain
  • skin rashes

Patient groups at risk for phosphate neuropathy and hyperphosphatemia are:

  • aged > 65 years

and patients with

  • CKD
  • dehydrated
  • bowel obstruction, delayed bowel emptying or active colitis and
  • on medications (diuretics, angiotensin converting enzyme [ACE] inhibitors, angiotensin, receptor blockers [ARBs], non inflammatories ( NSAIDs) and analgesics (opiates)

Preventing constipation particularly post operatively is vitally important. Being aware of your patients usual bowel habits and routines provides a baseline for the development of their bowel management plan.

“A stitch in times saves nine”

Negating the need to consider the use of enemas is a primary role of the nurse. Asking your patient “have your bowels moved today” is not a rhetorical question. Enquiring about the bowel activities of your patients is only the first step in preventing constipation. Doing something about lack of bowel movements is necessary.

Caution in use of phosphate based enemas for bowel cleansing pre procedure or for treatment of constipation is highly recommended. If administration is prescribed then nurses must be aware of patients at risk for hyperphosphatemia and phosphate neuropathy. Initiating a conversation with the prescriber regards the risks and clinical reasoning for your particular patient is necessary for their safety and wellbeing.

Adults fluid consumption impacts on risk chronic disease


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image66% of adults exceed the World Health Organisation (WHO) free sugar recommendation solely from fluid consumption.


A WHO study of 16,276 participants across 13 countries published in 2015 found that 66% adults exceeded the free sugar recommendation (free sugars <10% of total energy intake) from beverages alone without taking into account their food consumption.

Exceeding WHO recommendations for free sugar is associated with higher risks of

  • Weight gain image
  • Obesity
  • Metabolic syndromes
  • Type 2 diabetes and
  • other health problems

WHO estimates that by the year 2030 diabetes will be the seventh leading cause of death worldwide. Diabetes is associated with complications affecting the kidneys, eyes, feet, and cardiovascular system.

In Australia it is estimated that over 13% people with diabetes have lower limb nerve damage and 15% experience retinopathy. Diabetes is now considered the leading cause of end-stage kidney disease.

In people with diabetes, cardiovascular disease (CVD) is the primary cause of death, with around 65% of all CVD deaths in Australia occurring in people with diabetes or pre-diabetes. Furthermore, 41% of people with diabetes also report poor psychological well-being with reports of anxiety, stress, depression and feeling ‘burned-out ‘ from coping with their diabetes. Moreover, diabetes is ranked in the top 10 leading causes of death in Australia.


National Diabetes Strategy Advisory Group Consultation Paper

Risk of chronic kidney disease has already been demonstrated to be linked to the types of beverages consumed. Kidney Health Australia has adopted the viewpoint that there is

  • lack of evidence to suggest that drinking water in excess of thirst is beneficial
  • water is the preferred option to satisfy thirst
  • recommended fluid intake is proportional to thirst and individual circumstances
  • from the kidney perspective all fluids consumed counts towards the daily fluid intake and
  • drinking fluids when first sensation of thirst registers (thirst is a sign of dehydration)

Daily fluid intake is influenced by many factors. Fluid intake requirements are increased if

  • living in hot or tropical environments
  • increased activity and exercise
  • medical conditions causing excess obligatory fluid loss ie diabetes insipidus or conditions requiring increased urine flow ie renal calculi.

Fluid intake requirements are decreased in patients with end stage kidney disease and also those patients with certain cardiac and respiratory conditions ie cardiac heart failure.

Dehydration signs and symptoms include some of the following

  • headachesimage
  • fatigue and lethargy
  • slow reaction times
  • dark coloured urine
  • dry cracked lips.

Unfortunately fruit juice is still perceived as a healthy option despite the low water, high sugar content. Public health education programs encouraging adults to increase water consumption in preference to sweetened fluids so as to decrease their risk of chronic disease (ie CKD, T2DM, obesity) is required.

Nurses continue to play a significant role in educating patients and reinforcing health information. To be successful in effecting health change the message must be consistent, evidence based and current.

References :

Guelinck I, Ferreira‐Pêgo C, Moreno L A, Kavouras S A, Gandy J, Martinez H, Bardosono S, Abdollahi M, Nasseri E, Jarosz A, Ma G, Carmuega E, Babio N, Salas‐Salvadó J 2015 Intake of water and different beverages in adults across 13 countries Eur J Nutr 54 Suppl (2):S45-S55 DOI:10.1007/soo394-015-0952-8


Missed care by nurses impact patient safety

The incidence of missed care (of one or more cares) is 79% in even the best of work environments with a 92% incident rate found in the lower work environment deciles according to a 2013 study by Ball, Murrells, Rafferty et al.

Missed nursing care is considered  an error of omission defined as any aspect of required patient care that is omitted (either in part or whole) or significantly delayed. It first became recognised conceptually in 2006 in work conducted by Beatrice J Kalisch in the United States.

The quality of nursing care significantly determines (in part) patient outcomes. The patient safety in healthcare movement focuses on eliminating errors of commission (i.e. medications to wrong patient). Errors of omission (i.e. not ambulating a patient) are less detectable, problematic, more prevalent and detrimental than errors of commission.


imageSituations occur within the practice environment  causing a negative impact on nurses time availability for all of the cares required. Nurses at the bedside are very much aware of the care that they provide and those cares they omit.

The nature of providing nursing care lends itself to significant fluctuations in care requirements at any given time due to individual patient care requirements and demands. Flexibility and multi tasking are a necessary nurse characteristic in order to respond to these demands effectively.

Alarmingly there are increasingly more incidences where care needs to be prioritised, rationed or missed all together. Sound clinical reasoning and decision-making is required to ensure appropriate and safe decisions are being made most of the time.
Nursing is seen in healthcare budgetary terms as a ‘cost’ rather than ‘revenue’.


Increased restrictions placed on healthcare around the world mainly due to the global financial crisis is to reduce costs. Nursing labour resources is a significant drain on global health budgets making nursing a target for continual cost costing measures.
A negative correlation has been found between missed care and hours per patient day (HPPD) as well as registered nurse hour per patient day (RN HPPD). The higher the HPPD and RN HPPD the lower the amount of missed care.


There is no evidence in the literature that substitution of nurses with nursing assistants increases the rate of ‘missed care’. Studies conducted in medical, surgical, rehabilitation and intensive care units identified significant amounts of care being missed:

  • ambulation (84%)
  • assessing effectiveness of medications (82%).      image
  • patient teaching (80%)
  • mouth care (82%)
  • turning (82%)
  • timeliness prn medication (80%)

Interventions less likely to be missed include:

  • patient assessment each shift (17%)
  • glucose monitoring (26%)
  • hand washing (30%)
  • formal reassessment (36%)

One study in 2004 of frequency hallway ambulation by hospitalised older adults on medical units found that 73% of adult patients did not ambulate at all. This is despite clinical guidelines recommending the ambulation of adult inpatients at least three times each day.

Theoretically if ‘missed care’ could be reduced and surveillance increased would result in improved patient safety and better patient outcomes.

Patient satisfaction is accepted generally as a vital
indication of the quality of care provided.

Nurses, the care they provide and the organisational environment (cleanliness, meals) are strongly connected to patient satisfaction.Studies have demonstrated an association between nursing and patient satisfaction identifying nursing care as the only hospital service having a direct and strong relationship with overall patient satisfaction.

Other studies have found that patient perceived nurse caring is a major prediction of patient satisfaction. A 2011 European study of surgical patients spanning six countries reported that caring behaviours enacted by nurses determined a consistent proportion of patient satisfaction.

imageThe research is certainly out there that levels of HPPD and RN HPPD impact on rates of ‘missed care’, patient safety and outcome. Viewing nursing purely as a cost does not reflect ‘the whole picture’ on what appropriate levels of nurse staffing can have on healthcare budgets.

It could be argued that investing in nursing at the bedside in real terms by providing adequate staffing and skill mix whilst ensuring nurses have adequate resources at point of care will impact positively on the healthcare budget. Reduced adverse clinical outcomes, decreased length of stay, increased patient and staff satisfaction reduced errors of commission and errors of omission play a significant positive role and impact on healthcare costs.

Five questions nurses should ask prior to crushing medication:Legal implications


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An estimated 55% of drugs are administered unsafely according to 2015 Australian study Downey et al “Don’t rush to crush:audit of modifications to oral medicines for patients with swallowing difficulties”.

In the UK and Australia most drugs are “authorised for marketing” (licenced). The drug must be given (form, dose,ranges) according to its licence. Medical officers and pharmacists have legal authority to prescribe and dispense medication outside the drug license. Nurses do NOT have such authority. 

Altering the form of a drug (ie crushing) for many drugs is operating outside its licence. There are five questions nurses need to ask before proceeding with crushing medication.

1. Is there a valid clinical reason for the need to crush medications?

Patients experiencing difficulty with swallowing medication is common especially in the elderly. A nurse’s role in medication management is to ensure the patient receives their drugs as per the medication regime prescribed by a medical officer.

Crushing medications can destroy the physical and chemical properties of the drug. This can impact on the drugs effectiveness and potentially increase toxicity causing harm to the patient.

Individual preference, family pressure and ‘taking too long to swallow I don’t have enough time to stand here and wait’ are some reasons nurses might crush medications. These are NOT valid clinical reasons to crush.

Difficulty with swallowing (dysphagia) is a valid clinical reason considered appropriate for crushing medication. Nasogastric and PEG tubes being in situ are other valid reasons. If a patient is experiencing dysphagia they should be referred to a speech language pathologist for a swallow review and assessment. 

2. Is the doctor prescribing the medication aware of the nurses intent   to crush the drug?

Nursing concerns regards a patients swallow or requests from patient/family for crushing medication should be escalated appropriately. Assuming the medical officer and pharmacist are aware is not an acceptable response if decision to crush is challenged legally or professionally.

Medication management is a team effort. Patient/family, medical officer, nurse,
pharmacist and speech language pathologist are involved. Assessing and providing treatment for swallowing difficulties is important. A patient with a nasogastric or PEG tube for feeding purposes requires a comprehensive review of their medication regime.

Once a drug is prescribed and supplied outside of its licence (ie crushing in most
instances) the pharmaceutical company is no longer liable for potential side effects or harm. Clinicians making the decision to crush the drug is now liable for potential side effects or harm.

3. Are there alternatives preparations of the drug or alternative drugs available negating the need to crush?

Many drugs are not suitable for crushing ie slow release, enteric coated etc. With
increased technology and manufacturing processes it has become more difficult to determine visually if a drug is suitable to be crushed or not.

In many instances there are alternative preparations of a drug which bypasses the
necessity for crushing. Within each class of drugs are options a prescriber has in treating a condition. This allows the prescriber to choose a drug which has an alternative preparation which may be more suitable.

A conversation between the nurse, prescriber and pharmacist in most instances will be able to problem solve the issues involved without needing to crush the drug concerned.

4. Is the drug suitable to be crushed?

Some drugs are able to be crushed. The prescribing medical officer must be made aware the intent is to administer it by crushing. This needs to be clearly documented by the medical officer preferably on the patient’s medication order.

A valuable resource in Australia is a document “Don’t Rush To Crush”. This was developed in 2011 (and recently revised) by Society of Hospital Pharmacists of Australia. Additionally this text has been added to MIMS Online providing quick and easy access to all clinicians involved in medication management.

“Don’t Rush To Crush” provides comprehensive information of all oral solid drugs
available in Australia including if they can be crushed, the risks associated and how they should be prepared for administration to the patient.

5. Has the patient/family been informed of the risks associated with crushing of medications and provided consent?

Providing treatment and care outside of what is considered “usual care” requires patient consent. Consent includes providing the patient with the rationale/reason for the variance of care, the risks associated and alternative options available. Cushing medications would be considered outside usual care given the legal implications and risk for potential harm. 

The discussion and provision of consent should be well documented in the patients medical notes. The prescribing medical officer is responsible for the gaining of consent. Once a drug is NOT prescribed or administered in the form according to the marketing licence the pharmaceutical company is no longer liable legally for drug reactions.

The prescribing medical officer prescribing a drug outside of the marketing licence is legally liable for drug reactions.

A pharmacist providing a drug in the full knowledge it has been prescribed and/or administered outside of the marketing licence is additionally held liable for any drug reactions.

Nursing staff who crush medications without the knowledge of the medical officer and pharmacist is liable solely for any drug reactions potentially causing patient harm.

Providing safe nursing practice and care to patients is a nurse’s top priority. By asking these five questions of themselves or their colleagues prior to crushing any medication safeguards and protects patients and nurses equally.

Dementia Staging – Focus of Care


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In 2011 an estimated 298,000 Australians had a dementia and by 2050 this number is expected to triple.

People living with a diagnosis of dementia vary widely in their individual experience of symptoms and the progression of their condition.

Dementia is incorrectly thought of as a disease in its own right. Dementia is in fact a set of symptoms caused by several degenerative disorders.

Various stages and their descriptors have been developed in response to research and a better understanding of dementia. We now know the four most common types of dementia are:

• Alzheimer’s Dementia
• Vascular Dementia
• Dementia with Lewy bodies
• Frontotemporal Dementia (including Pick disease)

Less common is Creutzfeldt-Jakob Dementia and dementias associated with

• Huntington’s disease (HD)                         image
• Parkinson’s disease (PD)
• Alcohol
• Metabolic causes and
• Trauma

Staging dementia provides a guide for clinicians in determining the focus for treatment. In addition staging also helps in optimising communication among the person with dementia initially, the carers and clinicians.

There are multiple versions of dementia scales which ultimately increases the risk for miscommunication among all parties. The individual dementia scales have been developed focusing on a symptom or group of symptoms and progression through each stage is relative to symptom deterioration.

Alzheimers Australia provides information to health professionals and consumers describing a classical phasing system of Early, Moderate and Advanced Dementia. This scale is based on symptoms associated with cognitive decline although people with dementia do not experience all the symptoms within each of the phases. Cognitive fluctuations make it difficult to articulate clearly at which phase the person is in.

The grouping of symptoms within a four stage framework is described by Dementia Care Australia. This model is based on a social psychology construct rather than a medical one which is based on brain changes.

Progression through the four stages is relative to how the person with dementia is responding and interacting socially within their environment. Research has shown little correlation between brain changes and the symptoms and deterioration experienced by individuals with dementia.

The Clinical Dementia Rating (CDR) scale describes five stages of dementia progression and is based on a persons ability to perform in six areas of function and cognition:orientation, memory, judgement, home and hobbies, personal care and community. Stages are rated as no impairment, questionable, mild, moderate and severe impairment.

A common seven stage scale in assessing primary degenerative dementia is the Global Deterioration Scale (GDS). The GDS focuses on the amount of memory decline and is more relevant and useful in Alzheimer’s Disease (AD). It’s not as useful in some of the other dementias such as frontotemporal dementia as memory loss does not always occur relative to the progression of the dementia.

The descriptive language utilised in the stages and phases of dementia is prolific:early onset, pre-Alzheimers, early, middle, late, mild, moderate, severe,advanced and end stage. Any wonder clinicians find it difficult in clearly communicating with one another and consumers regard the extent of the dementia.

Australian health expert Dr. Jane Tolman describes a dementia scale in her work in this specialised field of healthcare. The model can be used in all types of dementia and has the ability to clearly articulate for clinicians the progression of decline. Focus of care underpins this three stage model.

The first stage is Dignity and Autonomy and the primary focus of care is to maintain independence and enjoyment.

Goal of care in the second stage is about Safety and maintaining quality of life often requiring 24/7 care either in a residential aged care facility or extensive support at home.

Providing Comfort and Dignity is the third and final stage. Symptom management and ongoing reassessment of the need for medications and interventions prolonging life, investigations which do not aide comfort and avoiding hospital presentations is the focus of care.

Just as with other dementia scales progression and the rate of progress through the three stages are variable and individualistic for each person.

Tolmans’ dementia scale is ideal for use in nursing practice and should be considered for use in acute, sub/non-acute and community settings. The focus of care at each stage independence, safety and comfort provide a clear direction for nurses to plan with family/carers ongoing care management for the person with dementia.

Dementia is a progressive and degenerative condition. The focus of care throughout the person/carers dementia journey is to plan for the inevitable palliative aspects of this disorder.

Malnutrition and Hypoalbuminemia – a predictor for illness prognosis


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40% patients are known to be malnourished on admission to hospitals in Australia. According to Australian Dietetics Association this increases to 70% in residents in Residential Aged Care Facilities (RACF). Malnutrition is clinically suspected in patients with a BMI < 18.5 and unintentional weight loss > 5% body weight.


Malnutrition is screened on admission to many Australian hospitals using the Malnutrition Screening Tool (MST) a simple three question tool designed for use by non-dietetic staff.  Patients are referred to Dietetics if they have a score >2 for assessment, review and implementation of a nutrition management plan.  Overweight and obese patients are similarly at risk for malnutrition and benefit from dietetic intervention particularly during times of illness and surgery.


General causes contributing to malnutrition are related to

  • inadequate oral intake (NIL by mouth peri-operatively, nausea\vomiting)
  • increased nutritional requirements (wound healing, pressure injuries)
  • impaired absorption
  • altered transport
  • altered nutrient utilisation


Malnutrition increases morbidity and mortality. Additionally malnutrition impairs functional recovery, increases muscle loss, impairs wound healing, increases the risk for infection and complications,  increases length of stays (LOS), affects quality of life and increases financial cost for hospitals and organisations. Significant oedema associated with decreased albumin blood levels impacts negatively on mobility and functional recovery. Hypoalbuminemia is also a predictor for morbidity more frequently cardiovascular morbidity, infection and organ dysfunction.

Albumin is a negative acute-phase protein which plays a major role in fighting infections, building and repairing muscle tissue. If the body is not taking in enough dietary protein the liver is less able to make new albumin further decreasing albumin levels. Normal range of albumin in blood is 3.5-5.5 g\l.  Maintaining levels of serum albumin within the normal range prevents the development of tissue oedema through maintenance of the colloid osmotic plasma pressure. The rate of loss of albumin to the tissue spaces (transcapillary escape rate) increases significantly when infection and sepsis if present.

A number of the more complex protocols that have been developed to detect malnutrition in adults rely on changes in acute phase proteins such as serum albumin and prealbumin as primary diagnostic indicators of adult malnutrition.


Monitoring albumin levels has been advocated as a prognostic tool to identify higher-risk patients because of the strength of the association and low cost of serum albumin assays. The acute-phase proteins—in particular C-reactive protein (CRP) may help identify the risk of infection or sepsis. Strong correlation between serum albumin and CRP with has been reported.

Studies suggest that administering sufficient exogenous albumin to achieve serum albumin level of more than 3.0 g/L lessens morbidity in hypoalbuminemia patients. Parenteral albumin solutions (200 or 300 mls of 20% albumin) have a good safety record. The ALBIOS study protocol stipulated that albumin administration should be titrated to maintain serum albumin > 3.0 g|l with albumin levels being measured on a daily basis.

Individual factors contributing to malnutrition

  • Age
  • Limited mobility
  • Inability to chew or swallow
  • Sensory loss (taste, smell)                                      th5R8LOT6Q
  • Lack of adequate intake
  • Apathy/depression
  • Treatment (ventilation, surgery, drain tubes)
  • Drug therapy
  • Inability to buy, cook or consume food

Organisational factors contributing to malnutrition

  • Failure to recognise malnutrition
  • Lack of nutritional screening or assessment disease (e.g., cancer, diabetes, cardiac, gastrointestinal)
  • Lack of nutritional training
  • Confusion regarding nutritional responsibility
  • Failure to record height and weight
  • Failure to record patient intake
  • Lack of staff to assist with feeding
  • Importance of nutrition unrecognised


Malnutrition and hypoalbuminemia corrective strategies include the screening of all patients on admission to hospitals for malnutrition with a full nutritional assessment for patients identified at risk.  Prescribing of oral supplemental high protein high energy drinks and frequent small meals of choice should form part of a nutritional management plan. Integration of new practises such as protected meal times provides the opportunity for staff to facilitate and monitor oral intake.

Regular blood analysis and review is recommended for patients considered high risk. Studies suggest that for post-operative patients an increased CRP level day 3 post op is a strong predictor for hypoalbuminemia on day 7.

Malnutrition and hypoalbuminemia continues to be unrecognised as such contributing factor in clinical deterioration of patients. Further awareness and education is needed for both nurses and medical staff if prevalence rates are to improve.

Salt – the good, the bad and the confusion


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75% of the daily consumption of dietary sodium intake are from prepared, packaged and processed foods. Added salt from the salt shaker accounts for a further 6%.

A successful Australian health promotion campaign in the 1970s was aimed at consumers to reduce salt in their diet during cooking processes and from adding additional quantities at the table for better health outcomes.

The word salt and sodium is used interchangeably in health language which has created some confusion within the community. Salt is made up of 40% sodium. Our body requires sodium for the maintenance of extracellular and serum osmolarity.

Excess sodium intake is excreted by the kidneys as sodium build up in the body is fatal. The kidneys excrete excess sodium more rapidly in the presence of higher blood pressure.

Sustained high blood pressure over a long period of time affects blood vessels by causing stiffening of the wall of the vessels. The damage to the blood vessels increases the risk for cardiovascular disease and stroke.

Sodium is naturally occurring in unprocessed foods – fresh fruimageit, vegetables, meat and dairy products. Australian dietary sodium recommendation for adults is 1.2 g/day. Currently the Australian adult daily average consumption is 3.5g/day.

Sodium does not act alone. Potassium works very closely alongside sodium. The ideal sodium:potassium ratio has not yet been clearly established, however it is thought to influence blood pressure more strongly than sodium on its own.

A study published in 2014 suggests that whilst a diet high in sodium (>6 g/day) is unhealthy, so too is a diet too low in sodium (<3 g/day). The ideal range of dietary sodium intake was considered to be between 3 g – 6 g/day.

A 2013 World Health Organisation (WHO) study found that almost all countries inhabitants exceeded the recommended sodium daily intake of 1.5g/day.

More than 25% of the world’s population over the age of 25 years suffer from hypertension. Hypertension is ranked as the leading cause of cardiovascular disease.

Concensus amongst hypertension experts is that the beneficial effect of salt reduction starts at daily intake levels of 5 gms or less and relatively high levels potassium in the low salt diets may have additional effects on
blood pressure.

Debate around sodium and salt intake is not around the effect on blood pressure and consequences to health, but around determining the right level of sodium intake to maintain optimal health.

Have Your Bowels Moved – Postoperative Constipation


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Constipation postoperatively is common. So too is the “have you moved your bowels today” catch cry from nurses everywhere. Many factors increase the risk for constipation in patients who have undergone a general anaesthetic.

Change in routine and diet, reduced fluid intake perioperatively, nausea and vomiting postoperatively, reduced mobility, pain, opioid medications and use and type of anaesthetic agents all have an effect on reducing gut motility increasing the risk for constipation.

Constipation is defined on the basis of stool frequency, stool consistency and difficulty passing stools. It is the accumulation of old hardened faces that is so tightly packed together that the bowel movements are infrequent and incomplete, causing much difficulty and strain, producing dry, hardened feces. The hardened feces will then stick to the walls of the colon and inhibit proper nutrient absorption.

Screening the patient prior to or on admission for chronic constipation is an important aspect to consider for minimising the risk for constipation. Ideally patients with a history of constipation should be flagged as high risk for developing constipation postoperatively.

Gathering information from the patient preoperatively is most likely to include their usual patterns of bowel movements, including the frequency, consistency, size or amount, and also amount or degree of straining when passing bowel motions.

A management plan could be implemented immediately paying very close attention to hydration perioperatively. Including the patient preoperatively in the development of their bowel management plan ensures that the patient has a voice in what works well for them. As part of developing the plan is patient education on risk factors which can exacerbate constipation.

Patients need to understand the importance of bowel movements in general and particularly postoperatively. Nursing staff can play a significant role in educating patients on appropriate level of fluid intake and the importance of moving and mobilising as much as possible. The use of the Bristol Stool chart is helpful in educating patients of appropriate stool consistency.

Postoperative nausea and vomiting (PONV) if not adequately treated can result in dehydration which impacts on fluid absorption and consistency of the bowel motion. Prolonged periods of fasting preoperatively has a similar effect if not adequately managed. The elderly are particularly vulnerable to perioperative dehydration.

Mobility restriction postoperatively due to type of surgical procedure performed and or pain adds an additional aspect impacting on constipation. Studies on the effects of physical activity in healthy subjects on colonic transit suggests accelerated transit time after physical activity . All patients should be encouraged to physically move as much as possible within the restrictions in place medically.

Optimising pain relief for mobility is a balancing act that is at times complex. Opioids reduce gastrointestinal propulsion and increases fluid absorption. Decreased mobility reduces gut motility. Ensuring the patient has the right amount of pain medication to maximise physical mobility is the goal here.

Medications may be used to assist in the prevention and treatment of constipation. Emollient stool softeners are easy to use and are best used prophylacticly in the short-term particularly for the patient receiving a postoperative opioid medication.

Many health professionals do not give bowel management the focus and the respect it requires. Constipation is uncomfortable and distressing for patients. Constipation postoperatively can lead to faecal impaction and gut obstruction which are possible serious consequences of untreated constipation.

Patient and staff education regards risks associated with constipation and how to prevent it postoperatively are the key to ensuring patients respond more often and with confidence “Yes my bowels have moved today thank you nurse”.