Category Archives: Clinical Care

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Key Elements When Designing and Delivering Effective Indigenous Falls Prevention Programs

05 Sunday Nov 2017

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Falls are now the second most common cause of injury for all Aboriginal and Torres Strait Islander people in Australia

Recovery post fall with serious injury (fractured neck of femur, head injury etc.) does require ongoing care and therapy to optimise functional outcome and quality of life. Rehabilitation and Allied Health services in the Australian general population have been reported to be too inflexible and difficult to access.

Indigenous people report often when trying to access mainstream healthcare of discrimination, judgment and communication problems.

When targeting aboriginal people for health promotion programs there are seven key elements which have been identified by indigenous communities as necessary if it will be accessed and be effective.

Indiginous Specific

A very consistent message is the need for the Health Programs to be indigenous specific. A lot of falls data is general populationrock-art-375225_640which has different demographics to ATSI population. Having the ability to modify the program to incorporate community specific variances that is important for that community.

Community owned

Kinship is a deep sense of family and community and is very strong amongst indigenous population. In communities everyone knows everyone and their family line. Self-determination is also strong in many communities. Preference is for an organisations/groups within the community to deliver any new program. Feeling safe to share their story and how they feel in a friendly environment is important for participants to interact.

No age limit

Along with Kinship is a need for the programs to have no age limit. That way children, carers and partners and family are welcome to attend. Family is not like family as in immediate family. Indigenous family is the community and a concept that whole of the local community is family.

Longer duration

Having a program that is of a longer duration so participants can drop out of and back in is required for any health promotion program. Things come up that prevents attending such as sickness, family reasons, and community responsibilities and the needs of country.

This six weeks or this eight weeks thing, it’s just no good for the Koori [Aboriginal] community because people get sick

 

You can’t offer Koori communities short term fixes because it doesn’t fix anything

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 Group based

Telling a yarn and sharing stories is the foundation of how Aboriginals interact with each other, as a community and the broader Australian community. Kinship is strong. Group based programs rather than one on one programs work best within this framework.

Low to no cost

Again the sharing of resources includes sharing of money. Health is high priority for the government and governmental agencies however for indigenous health is down low in their priorities. Indigenous communities are some of the poorest communities in Australia in terms of money. Preferably no cost programs are required to get people in and engaged.

Transport

Consideration for transport is also an important element which is also related to socio economic reasons. Even if people have a form of transport such as a car it may not be available due to sharing the car with family. Incorporating free transport into the program will remove a probable barrier and encourage greater participation.

Conclusion

Health programs specifically Falls Prevention require modification if wanting to deliver such programs within indigenous communities. Designing the program to be indigenous specific in a group setting factoring in low.no cost and transport is important. Opening the program up to all ages and deliver over a longer period allowing for drop out and in will be more effective with aboriginal communities. Aboriginal communities are best to deliver such programs from already established groups within the community. Underlying all these key elements are the principles of kinship, country and family.

Primary Resource

  1. Lukaszyk C, Coombes J, Turner N J, Hillmann E, Keay L,  Tiedemann A, Sherrington C &  Ivers R (2018)  Yarning about fall prevention: community consultation to discuss falls and appropriate approaches to fall prevention with older Aboriginal and Torres Strait Islander people BMC Public Health 18:77 DOI 10.1186/s12889-017-4628-6

Secondary Resources

  1. Australian Government Department of Health (2013) National Aboriginal And Torres Strait Islander Health Plan 2013-2023 Retrieved from health.gov.au ISBN: 978-1-74241-979-4
  2. Government of Western Australia Department of Health (2010) Falls Prevention for Aboriginal People A tool for Aboriginal Health workers and Aboriginal communities Retrieved from stayonyourfeet.com.au

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Understanding Conversion Disorder to better inform your patient sensitively

08 Saturday Jul 2017

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Conversion Disorder has had a name recently with the update of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) – Functional Neurological Symptom Disorder (FNSD).

The prevalence of FNSD is estimated to have a 1-3% occurrence rate in general population. In neurological outpatient clinics, the incident is thought to be as high as 25-30%.

“medically unexplained, neurological symptoms that are believed to develop
unintentionally in reaction to psychological and environmental factors
such as trauma or daily stressors.”

In previous years FNSD aetiology was believed to be anxiety/stress related. Sigmund Freud a 19th Century Austrian neurologist and founder of psychoanalysis theorised that anxiety is “converted” into physical symptoms.

More recent work in this area now suggests it has many interrelated and complex variables with or without an anxiolytic or stressful preceding event which makes treatment less than simple or a “one size fits all” scenario.

Diagnosing FNSD

Diagnosis of FNSD is considered clinically when all diagnostic testing is not compatible with presenting signs and symptoms. Misdiagnosis does occur although is less likely today due to significant advancements in diagnostics and research.

The DSM-5 diagnostic criteria for FNSD (conversion disorder) are as follows:

• One or more symptoms of altered voluntary motor or sensory function.
• Clinical findings provide evidence of incompatibility between the symptom and recognised neurological or medical conditions.
• The symptom or deficit is not better explained by another medical or mental disorder.
• The symptom or deficit causes clinically significant distress or impairment in social, occupational, or other important areas of functioning or warrants medical evaluation.

PNSD is more prevalent in women than men, rarely found in children or the elderly and has an increased rate in people aged the mid to late 30s. Patient populations considered more at risk are those with a personality disorder or dissociative identity disorder.

Hoover’s sign is a test available to clinicians when assessing limb weakness which with a positive result “simply suggests that the majority of the weakness you are observing is not due to disease”.

  Breaking the news

”The doctor just told me my stroke is all in my head”.
”I can’t move my bloody arm”.
“I’m not making it up”.
“I’m not crazy”.

A diagnosis of FNSD can elicit strong emotional reactions from the patient and family if not handled sensitively. Mental health illness still has a stigma very much attached. Commonly families and staff don’t know what to say or how to care for the patient which can isolate the patient more with feelings of stigmatisation.

Use of a standardised non-judgmental script and having confidence in responding to emotive and challenging questions “you don’t believe me?” is necessary for the diagnosis disclosure.

The information provided is just as important as the delivery in explaining the diagnosis to your patient. While the initial conversation is not necessarily a nurses role, the ongoing reinforcement and provision of information related to the diagnosis certainly are.

Communicating that PNSD is a significant health condition requiring a whole of team effort for the condition to improve and symptoms resolve and as per below:
• the emphasis that symptoms are genuine and potentially reversible;
• explanation of the positive nature of the diagnosis (i.e., not a diagnosis of exclusion);
• simple advice about distraction techniques, self-help techniques and sources of information;
• referral on to appropriate physiotherapy and psychological services; and
• offering an outpatient review

Treatment options available

  • The treatment plan found to be most effective is one with a motor learning program and a behavioural approach which is individualised within a multidisciplinary team environment.
  • Person-centred goal setting with the patient/family is recommended.
  • Behavior-oriented treatment strategies include unlearning maladaptive responses to eliminate example for the patients’ belief the limb is paralysed by informing them 1. that all tests indicate the muscles and nerves are functioning normally 2. the brain is communicating with the nerves and muscles, and 3. this apparently lost ability is recoverable.
  • Pharmacological treatment includes prescribing of antidepressants and anxiolytics if indicated.

Clinical Take Home Message

• FNSD is a significant health condition requiring a multidisciplinary treatment plan based on a motor learning and behavioural approach.
• FNSD has many interrelated and complex variables with or without an anxiolytic or stressful preceding event.
• Motor learning program with a behavioural approach which is individualised within a multidisciplinary team environment is most effective.
• Sensitivity is required when disclosing diagnosis and with ongoing communication due to stigma and spoken or unspoken sense of not being believed.
• Treatment options available include individualised motor learning and behavioural approach programs, anti-depressants, anxiolytics, education, and suggestive therapy.

Reference:
Carson A, Lehn A, Ludwig L, Stone J, 2016 Explaining functional disorders
in the neurology clinic: a photo story Pract Neurol;16:56–61. 
http://dx.doi.org/10.1136/ practneurol-2015-001241

Boeckle M, Liegl F, Jank R, Pieh C 2016 Neural correlates of conversion 
disorder: overview and meta-analysis of neuroimaging studies on motor
conversion disorder BMC Psychiatry,16:195 DOI 10.1186/s12888-016-0890-x

Septic Acute Kidney Injury – More than just Hypo Perfusion

02 Monday Jan 2017

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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

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

01 Saturday Oct 2016

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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 http://dx.doi.org/ 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).

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