Essay
Based on the clinical scenario below, list and discuss the possible diagnoses and explain the underlying pathology in relation to the presenting signs and symptoms.
What further information would you obtain from the patient and what other signs would you look for?
Outline the management and referral options, explaining your choice, and discuss any investigations needed to establish a diagnosis.
Scenario
Mrs Davies, a 39 year-old dentist, presents to your clinic complaining of a painful and swollen right elbow. This started 2 weeks ago and was first noted after a long session at the gym although she cannot recall any particular injury.
She is right hand dominant and the pain is starting to affect her ability to work and exercise. She has been on insulin since the age of 13 for type I diabetes mellitus and takes the oral contraceptive pill. She feels otherwise well.
Diabetes Melitus Type 1 (T1DM) is a metabolic disorder characterised by chronic hyperglycaemia. There is usually a sudden onset in childhood; also referred to as juvenile diabetes. T1DM is caused by an autoimmune reaction to the beta cells in the pancreatic islets of ODQJHUKDQ¶V which are responsible for insulin secretion (Ozougwu et al., 2013). These defects are possibly triggered by a virus or microorganism combined with genetic factors (Soedamah-Muthu, Abbring and Toeller, 2011). In T1DM, without insulin production to transport glucose from the blood to the tissues, glycogenolysis and lipolysis occurs resulting in: hyperglycaemia; increased protein glycation and Advanced Glycation Endproducts (AGE) in the tissues (Ahmed, 2004). Effects include symptoms of polyuria, polydypsia, dizziness, unexplained weight loss, polyphagia, fatigue, slow healing and blurred vision. Longstanding effects of T1DM may also lead to other organ specific autoimmune diseases such as hypothyroidism and rheumatoid arthritis. Long term pathological manifestations as a result of AGE include: peripheral neuropathy; nephropathy; retinopathy; atherosclerosis; angiopathy; poor wound healing and increased chance of infection (Graves et al., 2006).
Ahmed (2004), states that complications of prolonged hyperglycaemia appear to affect organs where cells do not need insulin for glucose uptake, such as the nervous system. Studies suggest that the interaction of AGE and their receptors (RAGE) alter intracellular signalling; gene expression and release pro inflammatory molecules and free radicals contributing to the pernicious effects of T1DM (Ahmed, 2004). An additional fact to consider is that long axons, distal to the cell body are more vulnerable to malnutrition and environmental insults. Together with sparse vascular supply and long term endothelial damage which occurs in T1DM, hypoxic nerve damage is also likely: resulting in peripheral neuropathy (Yagihashi, Mizukami and Sugimoto, 2011). It would be necessary to enquire whether Mrs Davies has recently be screened for peripheral neuropathy: which should be annually, five years after the initial diagnosis of T1DM (Kaufman, 2012). Prudent questions for the practitioner to ask relating to neural compromise include: is there any parasthesia or paralysis into the forearm or digits of the concerning hand? Which digits are affected? The practitioner should carry out a neurological examination to include: observation of feet for ulcers (as a result of sensory neuropathy and/or peripheral arterial disease); palpation for muscle tone/wasting and vibration/motor/sensory/proprioception testing for neurological deficit (vibration sensation is the first to be lost in peripheral neuropathy).
As a result of Mrs ‘DYLHV¶ T1DM, there will be a high propensity for peripheral neuropathy predisposing to median or ulnar nerve entrapment. Entrapment of the median or ulnar nerve may be due to vascular compromise causing compressive oedema or because of reduced biomechanics. The ulnar nerve is unprotected as it traverses between the humeral medial epicondyle and the forearm flexors which can be a common site for trauma or dysfunction. Special tests can be used to develop a diagnosis.
The medial nerve can be irritated as it passes between the two heads of pronator teres, possibly as a result of Mrs ‘DYLHV¶ dexterous occupation. Active Resisted Muscle Testing (ARMT) and other special tests may be diagnostic.
It is mindful to consider that nerve entrapment would cause muscle weakness and pain, however swelling would not necessarily be apparent as described by Mrs Davies.
Regarding peripheral neuropathy, T1DM patients may be unaware of micro trauma due to loss of sensation and Blackwell et al. (2014) highlight the common association between DM and olecranon bursitis as a result of this. Olecranon bursitis is characterised by inflammation of the olecranon bursa, with increased fluid within the bursal cavity- reflecting Mrs ‘DYLHV¶ symptoms of pain and swelling. Additional questions to glean more information include: what was she doing at the gym? Has she injured her elbow in the past? Does she have any associated manifestations in her shoulder/wrist/hand/fingers/neck?
Yari and Reichel (2014) report on the misdiagnosis of pyoderma gangrenousum as olecranon bursitis. Noting the relevance of asking questions relating to systemic health, it would be important to ask Mrs Davies whether she has suffered from any of the following: fevers, lethargy, unexplained weight loss and night sweats to assist the development of the working hypothesis and rule out infective or malignant origin.
The cardinal signs of inflammation: calor (heat), dolor (pain), tumor (swelling) and rubor (redness) are affected by enhanced circulating cytokines as a result of T1DM. Range of movement affected is also now considered to be a fifth sign of inflammation. Mrs Davies has reported of tumor and dolor. The practitioner would observe whether there is rubor and enquire whether Mrs ‘DYLHV¶ elbow is hot and if her range of movement has been affected. Using palpation, the practitioner could confirm the presence of calor and use Passive Range Of Movement (PROM) and Active Range Of Movement (AROM) to observe quality and quantity of movement of the elbow in comparison with the ³ZHOO´ elbow. It would be helpful to know which factors may be aggravating/relieving/nonaffecting to Mrs Davies- such as the use of anti-inflammatories, ice and rest. The character, intensity and daily pattern of pain would also be useful to know to develop a working hypothesis, as an inflammatory response is usually worse in the morning.
Other inflammatory conditions to consider include:
Rheumatoid arthritis (RA): a chronic autoimmune disease which has fluctuating severity and over time destroys joints- leading to dysfunction, deformity and disability (Stanaszek and Carlstedt, 1999). Questions related to Mrs ‘DYLHV¶ presentation would include: if there is stiffness in the morning that lasts longer than an hour? If Mrs Davies is experiencing bi-lateral pain in any other joints? Whether Mrs Davies has noticed any arthritic symptoms in her hands and fingers? The practitioner would palpate for any rheumatoid nodules commonly found over bony prominences (Stanaszek and Carlstedt, 1999). If RA were suspected, it would not be advised to treat Mrs
Davies osteopathically due to the inflammatory nature of RA. Therefore, a referral to Mrs ‘DYLHV¶
G.P would be necessary and further blood tests would assist diagnosis. Blood tests are positive for RA if there is an elevated erythrocyte sedimentation rate or if there is C-reactive protein, rheumatoid factor or anti-cyclic citrullinated peptide antibodies.
Psoaritic Arthritis (PA): another chronic autoimmune disease resulting from inflammation of the skin and joints. Questions to ask Mrs Davies to differentiate her presenting complaint with PA include: if she has psoriasis? Whether her toes and fingers are swollen (dactylitis)? If she has experienced any associated neck or back pain? The practitioner should also look for nail pitting and whether Mrs Davies appears to be generally fatigued. It would be important to refer Mrs Davies to her G.P with a hope to seeing a rheumatologist.
As Mrs Davies is a dentist it is necessary to consider the repetitive strains of her job resulting in tendonitis. To differentiate between the various tendons acting on the elbow, it would be necessary to ask Mrs Davies to point which part of the elbow is affected.
Tendons possibly affected include: triceps brachii as it inserts posteriorly into the olecranon; biceps brachii as it inserts anteriorly into the bicipital aponeurosis and the radial tuberosity; the forearm flexors pertaining to medial epicondylitis and the forearm extensors relating to lateral epicondylitis.
Pain elicited through ARMT would aid the development of a working hypothesis.
It is important to recall the effects of hyperglycaemia in T1DM; creating an increase in Reactive Oxygen Species (ROS), Tumor Necrosis Factor (TNF) and AGE which up regulate inflammation and impair matrix production reducing the tensile integrity of the tendon due to enhanced cell apoptosis and inhibition of collagen production (Graves et al., 2006).
Poor tendon health can also lead to Osteoarthritis (OA), which LVQ¶W considered inflammatory but a degenerative disease. King and Rosenthal (2015) explore the coexistence of OA and Diabetes Mellitus (DM). OA is characterised by the disruption of tissue homeostasis of the articular cartilage and subchondral bone and associated risk factors include; being female; advancing age; smoking; obesity and genetics (Ashkavand, Malekinejad and Vishwanath, 2013). With this in mind it would be necessary to ask Mrs Davies the following: if she smokes? Whether her parents have OA?
What she weighs?
Although Gramstad and Galatz (2006) highlight that elbow osteoarthritis typically affects men who engage in strenuous manual labour, it is important to recall the repetitive nature of Mrs ‘DYLHV¶ job combined with the deleterious effects of T1DM.
Biswas, Wysocki and Cohen (2013) explain that with OA of the elbow, pain is usually experienced at terminal flexion and extension possibly due to osteophytes, therefore further questioning into aggravating movements is necessary to develop differential diagnoses as well as enquiring if symptoms get better with rest. Biswas, Wysocki and Cohen (2013) note that primary osteoarthritis of the elbow is uncommon and highlight the importance of taking a detailed case history. It would be necessary to ask Mrs Davies if her elbow (or other body part) has been treated before by a doctor/physiotherapist/other complimentary/alternate medicine therapist? Is there any sensations of numbness and tingling in digits IV and V of her right hand? As ulnar nerve neuropathy can be a common finding in OA of the elbow (Biswas, Wysocki and Cohen, 2013). Other questions to be asked include: Has Mrs ‘DYLHV¶ had any accidents or operations?
Sundararaghavan et al. (2017) relate T1DM to decreasing bone density and increased susceptibility of bone fracture. This is probably unlikely in Mrs ‘DYLHV¶ presentation as there was no traumatic onset, however vibration test can rule out fracture. Zhou et al. (2015) state Charcott joint, referred to as neurotrophic arthropathy, is secondary to DM. It is reported that pain in the early stage of Charcott joint is not serious and may go unnoticed. Later stages develop increased pain, reduced range of movement and swelling (Zhou et al., 2015). A referral for x-ray would be necessary for diagnosis if Charcott joint was suspected.
If Mrs Davies was deemed safe to treat osteopathically, a conservative treatment approach would be advised, using non-direct techniques together with a suggestion to get a DEXA (Dual Energy Xray Absorptiometry) scan to assess bone mineral density.
Kolluru, Bir and Kevil (2012) highlight that T1DM can lead to Endothelial Cell Dysfunction, resulting in reduced Nitric Oxide (NO) production necessary for vasodilation; up-regulation of platelet aggregation; increased expression of adhesion molecules; an increase in circulating cytokines (increasing inflammation) and increased Reactive Oxygen Species (ROS) from the tissues. These factors influence the escalation of atherosclerosis and Venous Thrombo-Embolism (VTE). Hadi and Suwaidi (2007) and Tabit et al (2010) also concur that Cardiovascular Disease (CVD) is a major complication of DM. With respect to Mrs ‘DYLHV¶ presenting complaint, it would negligent not to consider that she may have a Deep Vein Thrombosis (DVT), resulting from T1DM effecting coagulation and fibrinolysis (Petrauskiene et al., 2005).
Enquiring which contraceptive pill Mrs Davies is prescribed would be necessary, as the Diabetes in Pregnancy Advisory Group (2010) recommend that women over the age of 40 with long standing diabetes should not take the combined oral contraceptive pill (OCP). As Usha Rani, Manjunath and Desai (2013) discuss, oestrogen and progesterone control the menstrual cycle in women which also affect blood glucose, progesterone in particular, further exaggerating the effects aforementioned of hyperglycaemia. It is also noteworthy to mention that correlations between oestrogen dosage and VTE are documented, resulting in hypercoagibility as a result of platelet aggregation, increased fibrinogen and coagulation factors (Bonar, 1987).
Pertinent questions to ask would relate to the :HOOV¶ criteria for DVT (1997) and with a score of two or more, Mrs Davies should go to A&E immediately to prevent possible myocardial infarction, pulmonary embolism or a cerebrovascular accident.
Other pertinent questions relating to cardiovascular health include: does Mrs Davies experience shortness of breath at rest/on excursion? Is there any chest pain? Is there any pain into the shoulder/jaw? Is there haemoptysis? Blood pressure, peripheral pulses and lower limb oedema should also be assessed.
To conclude, recognising the deleterious effects of AGEs on tissues and specifically the intima of the endothelial cells (Hadi and Suwaidi, 2007), it would be necessary to take Mrs Davies’ presenting complaint, without trauma quite seriously with referral to A&E with suspected DVT.
References
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