The Patient Discharge Plan

Dear Bloggers

Patient home discharges are as important as admitting the patient and getting the diagnosis and treatment correct.

As a medical student I was never taught how to assess a patient to plan for a discharge home. I assumed that it would be up to the decision from the senior doctor to decide whether the discharge home was appropriate. As I did my house officer years (residency) in the UK, through the many, many and sometimes tiring ward rounds, I was able to understand how the Consultants decided on how best to plan for a home discharge.

Young patients could usually be discharged on the day the Consultant gave them permission to leave hospital whereas with the elderly patients with mobility and social problems, I learned that a multi-disciplinary team was necessary to provide a safe transfer out of hospital to avoid re-admission because of failure to provide adequate supportive care. For example, elderly patients sometimes need a home visit with an Occupational Therapist to decide whether in fact the accommodation is safe or whether modifications need to be made to make the place more safe. Moreover, some patients who have no home support e.g. no family, need social worker advice to plan for home helpers or new accommodation.

Patients who have become weak after illness need rehabilitation to improve their activities. Sometimes, nutritionalists need to assess the patient to ascertain if calorific intake is sufficient.

All of these other modalities need to be considered in the elderly patients or those patients with special needs.

Hence, when the patient is admitted, it is worth considering when you are thinking of discharge home and what special services the patient is going to require. Hence, a plan can be organised early to engage such services so that the time can be used optimally. It is no good to just sort out the patient's pneumonia and at the end of it say that the patient can go home if they live in bad accommodation, have no support and can't walk properly.

However, patients who have no pre-morbid or social problems can usually be safely discharged as soon as possible.

I have heard of somewhat unusual examples as reasons for keeping patients in hospital and they include

• waiting for the the CRP or ESR to become normal
• waiting for liver function to completely normalise
• waiting for dose of prednisolone to become less than 30mg/day

I previously based my discharge of patients particularly on how they felt and how they looked by physical examination with of course taking into account investigative data. A patient with a recent pneumonia who has entered the recovery phase and is feeling well should not be kept in hospital just for the sake of watching the CRP. That is not a cost-effective reason and blocks an acute bed costing the patient and medical services more money with no particular evidence basis for keeping such patients in hospital.
The CRP in such patient is of course going to be raised, but it is the patient's clinical condition that is most important.

A patient with a raised ESR for polymyalgia make take several weeks or even months to decreased to an acceptably 'normal' level on steroids. Most PMR patient feel well within 48-72 hours of starting steroids and by keeping 'well' patients in hospital again serves no purpose.

Doses of steroids e.g. prednisolone >30mg/day is not a good reason for keeping patients in hospital. Yes, steroids are associated with many adverse side effects. However, if patients are well on their treatment and they have a good social structure and can attend regular outpatient appointments for assessment, then there is absolutely no reason to keep patients in hospital even on high dose therapy.

Patients mostly want to get back to some sort of normal home life, and the longer they remain in hospital the more institutionalised they will become. Moreover, the more they are kept in hospital, the more expensive it will be for them.

In addition, the more patients that you acquire on your medical service without discharging them, despite the fact that they are well, it will lead to the system becoming clogged up with well patients!

Well patients should not be kept in the hospital a second longer than is necessary.

Please consider....

Answers to Case: Patient with Fever, Headache and Sore Throat

Dear Bloggers

Here are the answers to the case from last week.

Question:

1) From just the history and physical examination, list the problems with this patient.

• Fever- low grade
  
• Headache- temporal and occipital location
• Sore Throat
• Tongue pain
• Restricted Jaw opening - TRISMUS
• Shoulder pain
• Fatigue / lethargy
• Lymphadenopathy
• Weight loss of 2kg
• Change in sense of taste and coated tongue
• Hepatitis C infection
• Raised AST & ALT + INR
• Normocytic Anaemia

2) Was there any indication to do a lumbar puncture in this case? Were there any contraindications? What is your interpretation of the result?

• Apart from the fever, there was no obvious indication to perform a lumbar puncture in this case. The patient despite having some headache said it was made worse when combing his hair. Meningeal pain does not worsen by touching the skull. There were also no meningeal signs from symptoms or physical examination. Moreover, there was an obvious relative contraindication that being the raised INR. In fact, an INR >1.4 is a relative contra-indication against LP until the coagulopathy has been corrected (see UpToDate 16.1-Lumbar puncture: Technique; indications; contraindications; and complications in adults).
  
• There is a real risk of puncturing a blood vessel leading to uncontrolled haemorrhage with the potential of causing spinal cord compression leading to paresis, from an extradural haematoma. However, if the need for a lumbar puncture is high, an experienced practitioner should perform the lumbar puncture with the aim of obtaining CSF on the first pass of the needle to avoid unnecessary trauma. Some practitioners recommend fluoroscopic examination to avoid puncturing small blood vessels.
  
• The LP results show that indeed there was trauma making the result somewhat difficult to intepret. However, in view that there are generally 1 white cells for every 1000 red cells, by scaling down the figures one would obtain a mildly raised neutrophil count. However, the LP was in fact repeated, which was again slightly traumatic and this revealed an otherwise normal white cell differential. Gram stain was again negative.

3) What other tests would you like to perform on the day of admission?

• In view of the above history, the diagnosis of Giant Cell Arteritis with Polymylagia Rheumatica is highly likely. Therefore, an Urgent ESR should be obtained. The patient also requires an Urgent Opthalmological Consult to look for retinal vessel occlusion which might be asymptomatic.
  
• Moreover, in view of the sore throat, throat swabs for streptococcus, adenovirus should be obtained. EBV and CMV levels would also be useful here in view of the lymphadenopathy, abnormal liver function and anaemia.
• Three sets of blood cultures should be obtained and and a cardiac echo performed.
• In view of the Hepatitis C infection, a mixed cryoglobulinaemia is a possibility although there are no skin ulcers, so obtaining cryoglobuilin levels would be useful for purposes of exclusion.
• Autommune Profile including ANCA, Rheumatoid Factor, ANA, etc
• TB PPD skin test could be performed and a chest Xray to look for typical TB shadows (there was no such problem in this case). Aiming to rule out TB should not delay the start of steroids in this severe vasculitic condition because of the risk of blindness and stroke. If TB is also considered likely and cannot be ruled out, then treatment for this should also be commenced empirically with the steroids until such tests rule in or rule out the infection, if indeed that is possible (See UpToDate 16.1- Major side effects of systemic glucocorticoids).
• Although this patient has Hepatitis C infection, starting steroids should not be delayed.
  

4) What is your diagnosis? What one test will provide the definitive diagnosis here?

• Suspected diagnosis was:

Giant Cell Arteritis with Polymylagia Rheumatica.

• An urgent temporal artery biopsy should be obtained.
  

5) What treatment would you start and when? How long do you continue such therapy and what other considerations are necessary?

• Oral prednisolone 40-60mg/day should be started immediately even before biopsy is taken because of the high risk of visual loss, stroke and dissection (please see UpToDate 16.1)
  
• Steroids should be kept at high dose for 2-4 weeks monitoring symptoms and ESR. Then slow tapering over 1-1.5 years
• Aspirin should also be given as it reduces the risk of stroke and other vascular events when compared to steroids alone.
• In view of high dose steroids plus aspirin, a proton pump inhibitor (PPI) should also be given to reduce the risk of gastric haemorrhage.
• Steroids can cause osteoporosis and consideration should be given to commencing a bisphosphonate on a weekly basis e.g. Alendronate 70mg. These drugs can also cause gastric irritation and so once a week dosing should be considered. This is yet another reason to provide PPI treatment.
• The patient should be monitored for diabetes and on discharge should be kept under regular outpatient follow-up and the patient should monitor their glucose by use of urinary test strips.
• Opportunistic infection should be considered in patients who are imunosuppressed by corticosteroids especially with doses >10mg /day or a cumulative dose > 700mg. Patients have a higher risk of pneumonia and infection with pneumocystis jiroveci. However, the risk is still small and hence, there is no current recommendation for use of Pneumocystis prophylaxis in patients on steroids alone (see UpToDate 16.1-Major side effects of systemic glucocorticoids )
  

Here is an excellent comment on the case from Dr Masami Matumura of Kanazawa University Medical School.

This case is difficult to diagnose, but challenging case.

Questions
1) From just the history and physical examination, list the problems with this patient.

I listed problems as follows;

1 Fever
2 Headache (which was worse when he combed his hair, suspect scalp pain)
3 Sore throat
4 Fatigue
5 Weight loss
6 Shoulder discomfort
7 Inability to open mouth
8 Impaired taste
9 Tongue pain
10 History of Hep C infection
11 Redness of throat
12 Lymphadenopathy
13 Anemia
14 Tachycardia
15 Tender temporal and occipital areas on the cranium
16 Tender in the neck

2) Was there any indication to do a lumbar puncture in this case? Were there any contraindications? What is your interpretation of the result?

I think there was no indication of lumbar puncture in this case. Because physical examination didn't disclose meningisumus. No neck stiffness, Kernig's and Brudzinski's signs were negative.
I think there were no contraindications for lumbar puncture. PT-INR was 1.52, slightly high. If meningitis is highly suspected, lumbar puncture should be performed.
Considering of the result of cerebrospinal fluid (CSF), traumatic tap is highly suspected. Because count of RCC in CFS was 1600. In this situation, I would order Indian ink stain. We can rule out cryptococcal meningitis.

3) What other tests would you like to perform on the day of admission?

I will order ESR and ALP in this case first. ESR must be high, approximately 100 mm/hour.

4) What is your diagnosis? What one test will provide the definitive diagnosis here?

My diagnosis is polymyalgia rheumatica (PMR) associated with giant cell arteritis (GCA)

Again my problem list is as follows;
1 Fever
2 Headache (which was worse when he combed his hair,
suspect scalp pain)
3 Sore throat
4 Fatigue
5 Weight loss
6 Shoulder discomfort
7 Inability to open mouth
8 Impaired taste
9 Tongue pain
10 History of Hep C infection
11 Redness of throat
12 Lymphadenopathy
13 Anemia
14 Tachycardia
15 Tender temporal and occipital areas on the cranium
16 Tender in the neck

Chronic inflammatory process is highly suspected by problem No. 1, 4, 5, 13, and 14. Collagen disease, infection, and malignancy should be differentiated. I would think problem No. 2, 3, 6, 7, 8, 9, 11, 12, 15, and16 are consistent with manifestations of PMR/GCA.
Another differential diagnosis is Sjogren’s syndrome associated with vasculitis. Problem No. 3, 8, 9, 11, and12 are manifestations of Sjogren’s syndrome. I have never seen a patient with Sjogren’s syndrome associated with vasculitis. But it is my one of differential diagnosis.
Another differential diagnosis is cryptococcal meningitis. This is less likely. I mentioned above.

I listed differential diagnoses as follows:

• PMR/GCA
• Sjogren’s syndrome associated with vasculitis
• Microscopic polyangiitis
• TB
• Cryptococcal meningitis
• Infective endocarditis
• Lymphoma

In this case, PMR/GCA is most likely. This patient is 70 years old man and discloses fever, headache (scalp pain), sore throat, fatigue, weight loss, shoulder discomfort, inability to open mouth (suspect claudication), tongue pain, anemia, tachycardia, tender in the neck, and tender
temporal and occipital areas on the cranium. Patient history and physical examination tell us the chronic inflammatory condition and characteristics of PMR/GCA. ESR is usually greatly increased in PMR/GCA. ALP is also increased in PMR/GCA.

Biopsy of the temporal artery is needed.

Criteria for the diagnosis of PMR/GCA is as follows;
(Bird, 1979)
1 Age > 65
2 Onset <>
3 Morning stiffness > 1 hour
4 Depression or weight loss, or both
5 Bilateral shoulder pain and stiffness
6 Upper arm tenderness
7 ESR > 40 mm/hour

If any three features, Sensitivity 92% Specificity 80%

5) What treatment would you start and when? How long do you continue such therapy and what other considerations are necessary?

I would want to confirm the existence of vasculitis and rule out TB. The possibility of TB is low, because the patient doesn’t have respiratory symptoms and abnormal findings in chest X-p.
Involvement of vessel may be segmental in patients with GCA, the diagnosis may be missed on routine biopsy. Serial sectioning of biopsy specimen is recommended. After the biopsy, glucocorticoid therapy should be started. Treatment should begin with prednisolone, 40 to
60 mg per day for four weeks, followed by tapering to a maintenance dose of 7.5 to 10 mg per day. This treatment should be continued for at least 1 to 2 years because of the possibility of relapse. If my diagnosis is correct, we can expect dramatic clinical response to prednisolone
therapy in this case.

The patient is 70 years old man. We should be careful of side effects of prednisolone therapy, especially opportunistic infection including pneumocystis pneumonia or cytomelgalovirus infection. Osteoporosis is another important side effect of prednisolone therapy in high aged patients. I would prescribe bisphosphonate to him when I start prednisolone therapy.

He has Hep C infection too. The existence of Hep C infection is not contraindicated for prednisolone therapy, however, we should monitor his liver function closely in steroid tapering phase.

Thank you very much for showing me interesting case presentation.

Thank you for such an excellent case commentary Dr Matsumura.

The result of this case indeed revealed the diagnosis of Giant Cell Arteritis with Polymyalgia Rheumatica. This was confirmed by a positive biopsy result.

Echocardiogram revealed no vegetation and blood cultures were negative.
Autoimmune screen was unhelpful with all major antibodies being negative e.g. ANA, ANCA

There was an unfortunate delay in starting the steroid therapy and the patient experienced some partial visual loss and unilateral numbness of his fingers and toes.
Opthalmological examination revealed occlusion of some of the retinal vessels.

Steroids were commenced immediately following this deterioration at a dose of 40mg prednisolone / day, and the patient's symptoms resolved before the result of the biopsy was known.

Moral of This Story

History and Physical Examination can give you the diagnosis to a case despite the difficulty of putting together the symptoms and signs. If GCA is suspected, steroids must be started immediately and not delayed because of the real problem of visual loss, as occurred in this case.

Delay potentially occurring to confirm the diagnosis by biopsy or the concerns about other diseases such as TB should not deter you from starting empirical steroid treatment for GCA. If there are concerns about other diseases such as TB, then empirical treatment should also be commenced for these until they are ruled in or ruled out.
GCA is one of those diagnoses where there are no 100% accurate tests and even the temporal artery biopsy can be negative.

Hence, you have to rely on what the patient says to you and what you find by examination and trust in yourself to have the confidence to start a treatment that can have many adverse side-effects by can also be not only sight saving but also life saving.

Please consider....

A Patient with Fever, Headache and Sore Throat

Dear Bloggers

Today, I bring you another most exciting case.

It is up to you to try and work out the diagnosis here.

A 70 year old male was see in another hospital's outpatient clinic with the following symptoms:

1. Fever
2. Headache
3. Sore Throat

Fever: The above symptoms had started gradually three weeks before. The fever was observed by the patient to be about 37.5 degrees and with slight increase above this in the evenings. There were no rigors associated with the fevers.

Headache: The headache had also come on gradually and was located in the sides of the patient's head and also at the base of the skull at the back. The headache was worse when the patient combed his hair. There was no associated nausea, vomiting, neck stiffness or photophobia. The patient denied visual disturbance and there was no limb weakness described. There was no history of a 'thunder clap' severe headache and no visual aura's.

Sore throat: The sore throat also started at the same time. The patient had been to see a local doctor and inspection of the throat revealed redness but no exudate. No throat swab examination was taken. An upper respiratory infection was favoured, and a 3rd generation cephalosporin was prescribed on that basis but no resolution of symptoms was observed.
The patient's symptoms were becoming progressively worse and he was feeling increasingly tired and had observed a loss of 2kg in body weight.

On further questioning, the patient was also experiencing shoulder discomfort and had in fact been feeling tired for almost 6 months. Moreover, the patient also complained of a recent inability to fully open his mouth. Also, his taste had become impaired. There was also confirmation that there was some tongue pain whilst eating food.

Body Systems Review

The patient denied joint and muscle pain and she described no swelling, no skin rashes, no cough / sputum / dyspnoea / haemoptysis / night sweats. There were no cardiac symptoms such as chest pain or palpitations. There were no other gastrointestinal symptoms such as epigastric pain / vomiting / constipation / diarrhoea / jaundice / change in colour of stool + urine / haematemesis / haematochezia. The patient had no obvious neurological symptoms.

The patient was a non-smoker and there was no history of contact with tuberculosis.

Previous medical history included Hep C infection following vaccination as a child.
There were no other medical problems.

The patient was taking no medications and there were no known drug allergies.

The patient was retired and lived with his wife in a 3rd floor apartment. There was a working elevator which had never had problems. However, when asked, he considered that it might take him several minutes to walk up the several flights of stairs if the elevator was to break because of fatigue.

On examination

The patient looked chronically ill but was fully alert and conversant.

HEENT: His tongue was coated with a thick white covering which was confluent rather than patchy. The oral mucosa was not coated. The throat was mildly red with no exudate. The thyroid was normal size and non-tender. There were several lymph nodes below the mandible bilaterally which were mildly tender, smooth and mobile. They were <1cm>
There was conjunctival pallor but no scleral jaundice.

Hands revealed no peripheral signs of systemic disease.

CVS: pulses were all present. There was a tachycardia of 100/min regular. JVP was not raised.
Heart sounds were normal with no murmur and no added sounds. There was no leg oedema and no evidence of deep vein thrombosis.

RESP: RR- 18/min, Sats 98% on room air, trachea central, no tracheal tug, normal percussion note and normal breath sounds.

ABDO: Soft, non-tender, no masses, no organomegaly, normal bowel sounds. Rectal examination was normal and revealed no faecal occult blood.
There was no jaundice and no signs of chronic liver disease.

CNS: Cranial Nerves 2-12 were normal. Taste sensation was not checked. Fundoscopy was not performed.

PNS: No neck stiffness, Kernig's and Brudzinski's signs were negative. Jolt accentuatuation was negative. Tone, power, reflexes, coordination and sensation were within normal limits.

Musculoskeletal Examination revealed tender temporal and occipital areas on the cranium. There was full range of movement of the neck but generally tender. There was no joint pain or swelling and muscles were non-tender.

Skin Examination: There was no obvious skin abnormality.

Bloods: revealed a normocytic anaemia with a haemoglobin of 8g/dl. Platelets were slightly raised. White cell count was slightly elevated at 12.1 x10^9/L. Liver function tests were three times normal for AST and ALT. HCV PCR was positive. INR was 1.52. Renal function was normal.

Urine: normal.

Lumbar Puncture was performed revealing RCC 1600, WBC 23 (neutrophils 15, Lymphocytes 8), normal protein and glucose. Gram stain negative.

CXR: Normal

ECG: sinus tachycardia.

Questions

1) From just the history and physical examination, list the problems with this patient.

2) Was there any indication to do a lumbar puncture in this case? Were there any contraindications? What is your interpretation of the result?

3) What other tests would you like to perform on the day of admission?

4) What is your diagnosis? What one test will provide the definitive diagnosis here?

5) What treatment would you start and when? How long do you continue such therapy and what other considerations are necessary?

The answers to this fascinating case will be provide in the near future. Please send me your answers so that they can be placed on the answer page.

Happy sleuthing.... :-)

Answer To Recent Case

Dear Bloggers

Here are the answers to the recent case.

Question 1: Taking into account the history and examination what other feature from the CBC do you think is abnormal in this case?

The other abnormal feature is the platelet count. In fact, she had only 3,000 per microlitre of platelets hence, Severe thrombocytopaenia. Her WBC count was normal, as was her haemoglobin and other coagulation studies.

Question 2: Why are her legs most affected and what is likely to be the likely diagnosis ?

Her legs were most affected because of the effect of gravity and venous pooling. The blood being under a column of pressure and with low platelets resulted in severe petechial haemorrhage.

In view of the recent infection, and no other sinister findings being found on examination such as lymphadenopathy, the suspected diagnosis was a viral induced thrombocytopaenia. ITP was also considered strongly in view of the patient's presentation, her female gender, a normal sized spleen and absence of other symptoms.

Of course, malignancy e.g. MDS, leukaemia, other autoimmune diseases e.g. SLE, were considered, but in view of an otherwise normal blood differential and no other features consistent with these pathologies, they were not really considered to be likely as the cause.

Question 3: Why might the BUN be raised?

The BUN may have been raised because of asymptomatic gastric haemorrhage.

Question 4: Would you admit this patient into hospital even though she feels well or would you let her go home?

This patient is high risk for parenchymal haemorrhage. Initially, low platelets results in cutaneous petechiae. If the platelet count worsens, then mucosal bleeding occurs. At this point, one should be highly suspicious of potential severe bleeding ensuing e.g. intracranial haemorrhage, GI bleeding.

Hence, the patient should not be sent home and should be admitted to hospital for investigation and prompt treatment.

Question 5: What other tests would you like to perform?

• The patient should have viral titres taken e.g. Adenovirus, Parvo Virus, Hep C, CMV, EBV, Mumps, Rubella Autoimmune profile e.g. Anti-DS DNA, ANA Abs for SLE
• Blood smear to look for abnormal cell morphology
• Anti-platelet antibodies (if available)
• Bone Marrow Examination-- essential to aid in the diagnosis
• Ultrasound of the abdomen to look for splenomegaly
• Ultrasound of the knee to look for haemarthrosis-- aspiration is not safe with profoundly low platelet counts.
• Rectal examination for occult bleeding (easy to do and often avoided!!)
  
• Gastroscopy and colonoscopy
  
• Treatment here would be to transfuse platelets and treat the underlying cause (if known)

The bone marrow examination revealed: increased numbers of megakaryocytes of normal morphology. There was also a slight increase in the erythroid precursors.

The serology revealed: a normal panel autoimmune profile e.g. normal levels of ANA.

Her viral serology showed past infection with CMV and EBV and Parvovirus and HCV were negative. Other viral serology was unfortunately no performed.

Abdominal ultrasound revealed a normal spleen.

Anti-platelet antibodies were positive with a level of 75 (normal <5).

Hence, in view of the clinical history, physical examination, the bone marrow examination and positive anti-platelet antibodies, it was considered that the diagnosis was:

Immune Thrombocytopaenic Purpura.

She received prednisolone at a dose of 1mg/kg/day -- 50mg in total, and her platelet count increased to 30,000 within 3 days with no new bleeding problems. However, despite high dose steroids, the platelet count did not increase much beyond this level thereby prompting the use of other treatment modalities (see description and treatment of ITP below)

Here is a most excellent response from Professor Masami Matsumura of Kanazawa University School of Medicine with his opinion on the case.

This is interesting case for approaching the diagnosis.

ID/CC: 50-year-old woman with a diffuse skin eruption

Problem list:

1. Episodes of URTI
2. Diffuse skin eruption, suspect petechiae
3. Oral mucosal bleeding
4. Left knee acute monoarthritis without trauma history
5. Oedema of both ankles
6. Mildly raised BUN (20.1)
7. Mild monocytosis
8. Mildly raised CRP

Assessment:

After episodes of URTI, she had left knee acute monoarthritis, diffuse skin eruption, and oral mucosal bleeding. These issues are consistent with Immune Thrombocytopenic Purpura (ITP). Another differential diagnosis is Henoch-Schonlein purpura. Acute polyarthritis is observed in this disorder. However, oral mucosal bleeding is not observed in Henoch-Schonlein purpura. Moreover, palpable purpura is characteristic of this disease. I think ITP is most likely in this case.

Another differential diagnoses are follows:

• Hematologic malignancies including CLL
• MDS
• SLE
• Viral infection including hepatitis C and HIV
• Evans’s syndrome

Question 1: Taking into account the history and examination what other feature from the CBC do you think is abnormal in this case?

This patient has mucosal bleeding. I think her platelet count is under 10,000/m(micro)L.

Question 2: Why are her legs most affected and what is likely to be the likely diagnosis ?

Her physical examination revealed acute monoarthritis in left knee. When we see acute monoarthritis, Gout, Pseudogout, Infectious arthritis, Bleeding, and Trauma (PIG TB is my mnemonics) must be differentiated. She denied trauma episode. Bleeding is most likely in this case.

Question 3: Why might the BUN be raised?

I suspect GI tract bleeding. GI tract bleeding can cause elevated BUN.

Question 4: Would you admit this patient into hospital even though she feels well or would you let her go home?

This patient must be admitted into hospital for close examination and treatment!!

Question 5: What other tests would you like to perform?

• Fundoscopy for examination retinal bleeding
• Peripheral blood cell morphology for detecting large platelets
• Coagulation studies including PT and APTT
• ANA, HCV antibody assay
• Abdominal echo for evaluate spleen size
• Bone marrow aspiration

An anonymous response was received as follows:

1.? Platelets>low; stool occult blood +
2. Henoch Schoelein, Behcet [pathergy from your History], Parvo 19, R/O DVT, anti-phospholipid syndrome
3. ^ BUN from GI bleed
4. In Japan, admit; in North America follow-up in clinic
5. Skin Bx, Fiber Colon/gastro filber if stool blood +; L knee OA

Immune Thrombocytopenic Purpura (ITP)

This is a bleeding disorder resulting from low platelets not associated with another systemic disease. For the diagnosis to be made, other disorders should be excluded through other tests. Autoantibodies are usually produced against the platelet resulting in the low platelet level. In children, a viral infection can also result in ITP.

The spleen is usually normal size except if there is co-existent viral infection.

The symptoms and signs are of petechiae and mucosal bleeding e.g. in the mouth, GI tract etc. Examination of the blood reveals an isolated reduction in platelets but an other normal morphology and differential of white cells and red levels.

Bone Marrow examination reveals normal or increased numbers of megakaryocytes with other bone marrow elements being normal. Other pathologies should be excluded as described above and HIV testing should be performed in those individuals considered to be at risk because this infection can appear in an identical way to ITP.

Treatment consists of corticosteroids e.g. Prednisolone 1mg/kg/day. In those patients who respond to treatment, the platelet count should increase to normal in 2-6 weeks. The steroid dose is then tapered accordingly. In patients who do not respond to treatment and in who have a high risk of haemorrhage, splenectomy is considered.

Other immunomodulatory treatments are sometimes used such as immune globulin transfusions, cyclophosphamide, azathioprine and the anti-CD20 antibody (Rituximab).


Many thanks for all those doctors who contributed to give their opinions on this case.

There will be more great cases coming....stay tuned!!! :-)

A Case For You To Answer

Dear Bloggers

This case was provided to me by another physician and it has been anonymised for purposes of confidentiality.

A 50 year old female was seen in another hospital's out patient clinic because of a diffuse skin eruption.

She had been mildly unwell for 2 months with symptoms of an upper respiratory tract infection, the symptoms that included sore throat, mild fever, chills and nasal congestion. He was initially seen and given acetaminophen and multivitamins. Her throat examination at that time was red but with no exudate. No antibiotics were prescribed. No throat swabs were taken.

Her symptoms initially improved but there was a recrudescence of the same symptoms prompting a return to the hospital outpatient clinic. Again, medications for control of symptoms were prescribed and no antibiotics.

Two weeks before her current presentation, the URTI symptoms had completely resolved and she was feeling otherwise well.

However, after several days, her left knee began to hurt and she found it difficult to walk properly. There was no apparent swelling of the joint or preceding injury as mentioned by the patient.

A reddish-blue eruption began to emerge on her arms, legs and trunk. The eruption was composed of apparently very small areas of haemorrhage which were non-blanching and over approx 1-2m in diameter. The worse affected areas were her lower limbs. She also described other areas erupting after scratching her skin.

She denied visual disturbance, headaches, rectal bleeding or haematuria. Her other joints were non-painful.

She had described noticing blood in her mouth when cleaning her teeth and recent nose bleeds when blowing her nose hard several days before admission.

Previous medical history was nothing in particular apart from seasonal rhinitis.

She was taking no medications

She had no relevant family history and was a non-drinker and non-smoker.

On further questioning, she had no weight loss, a good appetite, no night sweats. No abdominal pains or other GI symptoms. In fact, she was otherwise feeling well.

On examination

Temp 36 C, Pulse 80 regular, BP 120/80, RR- 12, Sats 98% on RA. No Jaundice, Anaemia, Clubbing, Cyanosis, or Lymphadenopathy (JACCL)

She looked well but had a diffuse rash (as described above). Mouth- blue-black raised vesicle on the right lateral border of the tongue and on the buccal mucosa bilaterally. Elevation of the tongue revealed fresh blood in the lateral gutter at the junction of the floor of the mouth and the medial aspect of the gums.

CVS: JVP not raised. Heart sounds were normal. No evidence of DVT.

RESP: Percussion resonant, breath sounds vesicular.

ABDO: Soft, non-tender, no hepatosplenomegally. No ascites. Bowel sounds increased. Rectal examination not performed.

Left knee- mildly swollen. Not warm or tender. Bruising over infra-patella region. No patella tap. Crepitus on extending knee joint.

Oedema of both ankles.

Initial screening bloods were entirely normal except for a mild monocytosis, mildly raised CRP and BUN (20.1) but normal creatinine PLUS one other feature.

Question 1: Taking into account the history and examination what other feature from the CBC do you think is abnormal in this case?

Question 2: Why are her legs most affected and what is likely to be the likely diagnosis ?

Question 3: Why might the BUN be raised?

Question 4: Would you admit this patient into hospital even though she feels well or would you let her go home?

Question 5: What other tests would you like to perform?

PLEASE SEND IN YOUR ANSWERS BY POSTING THEM ON THIS BLOG ANONYMOUSLY AND THE CASE RESULT WILL BE AVAILABLE IN THE NEAR FUTURE.

Clinical Skills

Dear Bloggers

Now is the season when medical students visit various hospitals around Japan for a 3-day period to see what each institution has to offer for the purposes of future training in the respective residency programmes.

In Japan, most medical students do not have any clinical 'hands on' experience until the beginning of the 4th or 5th year of medical school.

From my previous interactions with several students and residents at different institutions, the general consensus is that the teaching of clinical skills at university is not optimal for what they need to examine patients. Of course, some medical schools have many sessions for teaching on real patients and there is the newly introduced OSCE system to ensure that there is a basic minimum standard. Hence, training can be variable depending on the institution in question.

Some UK medical schools have the medical students learning clinical skills from their very first year by placing them with a community general practitioner who can select for them well patients with chronic illness, who attend the clinic to have their history taken in full in addition to examination by the student. The general practitioner then listens to the history and demonstrates the examination to reinforce good practical skills and to advise on additional history which can help to make a bedside diagnosis.

My medical school was one of the first to do this in the UK and that was nearly two decades ago.

Although the basic knowledge of medicine was still to be learnt, by intercalating the learning from each system, over time it was then possible to gain deeper understanding plus having the background knowledge of how to examine for signs.

Hence, when it comes to the official clinical years, which start from the third or fourth year in the UK system, the medical student already knows the basics such as percussion, auscaultation etc...

One method that is very informative is the ward round system and listening to the consultants taking extra history and examining the patient. The UK medical system is somewhat adversarial in its way towards medical students because invariably they get picked on to be asked the various causes of XYZ disease or how to examine for ABC sign. Although this can sometimes be a stressful process, it forces the medical student to read about the patients they see. Moreover, the consultants invariably ask the medical students again at various stages of their attachment to a firm. Knowing the answer shows that medical student has taken the time to find out what the consultant wants to know.

By joining ward rounds and seeing the patients 'hands on' is the best way to learn clinical skills rather than just from a book in the class room. Patients do not write the books and there can be any number of possible combinations of acute and chronic diseases to provide a challenge to the doctor. This cannot be found in detail to any great extent in a book.

To really understand clinical medicine, you have to do clinical medicine.

Although these 3-day snap shot visits by medical students provide a mere glimpse of how hospital life operates, it is in my opinion, insufficient to learn new clinical skills.

At this hospital, there is the opportunity to do short term externships of several weeks to a month whereby the medical student can be exposed to the daily rigors of clinical medicine and how to treat the common acute problems and the difference of how to treat chronic diseases.

They get the opportunity to take histories from patients and to learn clinical examination in depth.

Such students who have done this in the past with me have learned a lot and their experiences have been very positive.

If you are interested in such an externship at this institution, then please contact me at the email address at the bottom of the blog page.

The Breast Examination

Dear Bloggers

I am a general medicine physician, not a surgeon, but it is essential to still know how to do a breast examination.

Although there are time constraints in the very busy Japanese outpatient clinics or ER departments, patients should nevertheless be asked if they have any breast problems and whether they check their breasts by themselves.

Moreover, if a female patient presents with chest pain, bone pain e.g. back pain, pneumonia or even an ovarian mass, the breasts should be examined.

There seems to be an aversion to performing breast examination especially by male junior doctors because of the age difference or even age similarity between the doctor and the patient. This should however, not prevent breast examination being performed, as it is the patient's health that is most important and not how the doctor feels. However, there are ways to make the breast examination less stressful to perform such as providing privacy by ensuring the curtains are pulled around the bedside or across the clinic examination area. Staff should be informed not to open the curtains when coming in, if indeed they actually need to come in! In fact, limit the number of people allowed to enter during the examination unless the patient has given permission. Ensure you have a nurse chaperone and that your hands are warm! Ensure that the patient is covered over whenever you are called away and when you finish the examination.

Any patient who requires a breast examination, as a doctor, you should ALWAYS take a female nurse chaperone with you so that they can observe that the examination is done correctly and that the patient and the doctor have a witness for legal purposes. Never do an examination unaccompanied.

When you eventually write your hospital notes, write down the name of the nurse chaperone as well so that you have a record of who was in attendance-- again for legal purposes.

So, how is the breast examination done?

Well, it is relatively straight forwards. First of all, GET PERMISSION FROM THE PATIENT !! You then expose the anterior chest to expose both breasts for means of comparison. Look at the skin to see if there is tethering and the classical 'peau d'orange'-- the peel of an orange, which can be a presentation of Ca breast. Look to see if there is nipple retraction. Ask the patient if the retraction, if found, is new or long standing. Some patients have naturally occurring nipple retraction, but if new, it is an ominous sign of potential malignancy.

Look at the skin colour, does the breast look inflamed? Some malignancies spreading in the surface of the breast can give a red inflamed appearance although the differential diagnosis would be an infective mastitis or even radiation exposure if there was a previous history of breast or lung cancer that had required radiotherapy.

Next, begin the palpation in the outer quadrant of the breast where the axillary tail exists. A significant number of cancers can present in this outer quadrant and can be missed by the inexperienced doctor. Palpate with both hands in each quadrant to see if the breast tissue is uniform and whether it is firm or soft. Feel to see if the breast tissue is mobile, which is normal, or fixed, the latter which is again, another sign of potential malignancy. Ask the patient if the examination is painful or not. Remember, that breast tissue changes according to the menstrual cycle with changes in female hormone levels, so tenderness may vary.

Next examine the nipple area for discharge by gently squeezing the base of the nipple. Discharge of sanguinous fluid is again another ominous sign and should alert the doctor of potential malignancy. Mucinous discharge may also be of significance.

Next, examine the axillary and cervical lymph nodes for size, consistency and mobility.

Look at the upper limbs to determine if there is any swelling of either arm and any dilatation of the veins on the arm and upper chest. Some advanced tumours can cause subclavian-axillary vein thrombosis which is a serious complication. If advanced malignancy is found, listen to the chest, palpate the bones if the patient complains of bony tenderness, perform a neurological examination e.g. brain metastases, acute cord compression, and feel the liver and other abdominal and pelvic organs. Remember that Ca breast can spread to the ovaries producing the infamous Krukenberg tumour.

If you do find anything abnormal on examination, consider asking for a surgical consultation, as such masses usually require ultrasound examination and needle aspiration or biopsy examination.

Consider checking a chest xray, and other relevant radiology depending on the examination findings plus the alkaline phosphatase, calcium and liver enzymes.

If you do not ask patients if they have breast problems then you may miss a potentially treatable problem. Some patients will not offer up that they have a breast problem unless asked. A recent patient at another hospital presented to the doctors with a breast mass that had been evolving over several years. She had not disclosed the problem to anyone and unfortunately, the malignancy was already producing end-stage problems, and hence, a curative procedure was not possible.

Just as junior doctors are not inclined to perform rectal or genital examinations, along with these, you should encourage your self to also perform breast examination whenever clinically justified because it is a part of the general physical examination that is unfortunately all to often ignored because of embarassment.

Please consider.....

Atrial Fibrillation and its Management-- the hard facts

I have talked of Atrial Fibrillation (AF) on this blog in the past, but today I think it is helpful to revisit this common disorder to discuss the correct management.

The causes of AF are well documented and I do not intend to go into any depth here, but common things being common, infection, valvular disease, ischaemic heart disease, heart failure, pulmonary embolism, thyrotoxicosis and electrolyte disturbance are what are considered the main causes.

Although treating the underlying condition may eventually ameliorate or resolve the AF e.g. Thyrotoxicosis treatment, the acute AF at the time of its presentation should be treated.

Why should AF be treated at all?

Well, AF causes disordered and rapid ventricular contraction and as a result there can be a loss of 10-20% of cardiac output (CO). In fact, this can worsened yet further in the elderly with as much as a 40% drop in CO thereby precipitating heart failure.

Moreover, studies have shown that there is a 2 x increased mortality overall from AF.

The presence of AF, especially in the elderly, can precipitate Heart Failure and ironically, heart failure can also cause AF ! It is the Chicken and the Egg phenomenon.

Fast AF can also result in rate related ischaemia and patients can develop acute coronary syndrome with rise in Troponin T, the most sensitive of the current cardiac biomarkers. I have seen this occur in many British patients.

The reduction in CO can also result in hypotension and cause patients to collapse.

Of equal importance, AF can result in thromboembolism and vascular occlusion e.g. Limb ischaemia, stroke, renal infarction.

Hence, whereas in the past AF was looked upon as some inconvenience for the patient but an otherwise benign condition, it is now recognised to be a serious cardiac disorder that requires immediate treatment.

The American Heart Association and European Resuscitation Council Guidelines ALL advocate immediate treatment for

• Control of rhythm / rate
• Anticoagulation

especially if the patient is unstable e.g. developing heart failure (please see European Guidelines above).

Moreover, AF should not just be assumed to be as a result of, for example, infection, without ruling out the other common causes e.g. MI, thyrotoxicosis, heart failure, electrolyte disturbances.

Treatment

If the patient is haemodynamically unstable (i.e. hypotensive) because of the Fast AF, then these patients should receive electrical cardioversion unless contraindicated e.g. Unfit for anaesthesia.

Haemodynamically stable patients should be treated with either rate control or rhythm control therapy although this depends on what you as physicians wish to achieve for your patients in the long term. There has been shown to be no difference in outcome between rate control or rhythm control, and in the vast majority of patients, rate control may be easier to achieve in the long term than hoping to maintain sinus rhythm.

For example, a young patient with no structural heart problem with onset of AF (Lone AF) e.g. caused by alcohol, has a greater chance of being reverted to sinus rhythm than for an old patient who may for example, have ischaemic heart disease or enlarged atria. Hence, rhythm control by chemical cardioversion, or even electrical cardioversion either within 48 hours of onset of the AF or at 4-6 weeks after combined chemical cardiovertor therapy e.g. Oral amiodarine, plus anticoagulation with warfarin can be used.

If your goal is for rate control e.g. In the elderly patient with congestive heart failure, then treatment will differ in that drugs for rate control rather than rhythm control can be used e.g. Beta blockers, digoxin, diltiazem. However, in the elderly the choice of the best drug to treat AF is also determined knowing whether the patient has heart failure, liver failure or renal failure.

In severe heart failure calcium channel blockers e.g. Verapamil can worsen CHF by reducing cardiac muscle contractility and should be avoided in patient with a low ejection fraction e.g. 40%, whereas drugs such as digoxin and amiodarone do not deterimentally affect myocardial function.

However, in liver disease, long term amiodarone therapy may cause worsening liver function.

In renal failure, digoxin levels can rise and cause toxicity which includes nausea, vomiting, colour vision changes and profound bradycardia. Digoxin toxicity can also be made worse by hypokalaemia and hence, patients need levels of digoxin performed plus monitoring of potassium. Often patients are also using diuretics that can cause hypokalaemia and hence, polypharmacy and drug interactions should always be borne in mind when prescribing such drugs.

Thus, drug therapy for AF requires a knowledge not only of the the indications and pharmacotherapeutic effects but also of the side effects and hence, the contraindications.

So, in summary, fast AF should always be treated actively.

Rate control and rhythm control have a similar overall outcome and hence, the only choice between such therapies lies in symptom control, as restoring sinus rhythm is associated with less symptomatology.

Treatment of AF consists of either electrocardioversion, or pharmacological treatment. Pharmacological therapy consists of rhythm controlling or rate controlling agents.

Anticoagulation should be commenced acutely with heparin and then converted to warfarin. Lone AF, where a structurally normal heart exists in a patient <60>

Paroxysmal AF has the same risk for thromboembolism as continuous AF and hence, anticoagulation should be provided.

Using asprin instead of warfarin is associated with a higher thromboembolic risk but this is better than no anticoagulation at all. It may sometimes be better to use aspirin in the falling elderly patient with AF instead of warfarin because there is a potential risk of head injury and hence, subdural haemorrhage. Basically, it is a trade off between reducing severe bleeding complications but achieving some form of anticoagulation.

If possible, discuss the pros and cons with the patient; they should be given the choice rather than the doctor being paternalistic and choosing for them, as anticoagulation with its many benefits does not make the patient feel better, but can cause life threatening bleeding. Remember, it is their life and they should be involved in making decisions that may affect their health.

Please refer to any of the famous texts such as Harrison's, Merck Manual, UpToDate, and of course to the American Heart Association and European Resuscitation Guidelines (above) for a more in-depth discussion of AF.

Please consider...

Professor Stein-- is back!

Dear Bloggers

Last week saw the return to our hospital of Professor Stein from Florida, USA.

Prof Stein spent 3 days going through daily cases and teaching the internal medicine residents with particular focus on history taking in order to consider the diagnosis before seeing the patients at the bedside.



Various cases were presented including a recent case of Tetanus, Miliary TB, Castleman's Disease and psoas abscesses with additional vertebral infection.

There was the excellent chance of a combined meeting with Prof Stein, the US Navy Hospital from Yokosuka and our institution. This meeting generated direct and frank discussion of the cases, the likely causes and the management.

In all, the 3 day whirlwind tour was an excellent opportunity for the residents to present their cases to a distinguished Professor of Medicine in English and to hear his words of wisdom.

A Challenge For You All--- the Answers!!!

Dear Bloggers

Over week has passed since I extended the answer limit for the Challenging case I set a few weeks ago.

Following are what I regard to be the answers to the case.

In such a case it is essential to have a problem list which details the important elements of the history, examination, laboratory and radiological data in order to try and understand the problem.

Problems from History

• Vomiting and Diarrhoea
• Reduced conscious level
• Cardiac arrest
• PMH of Parkinson's disease and constipation
• Drugs- for PD, tricyclic antidpressants, senna, Aricept
  

Problems from Examination

• Hypotension, Bradycardia, small volume urine (dark colour)
• Hypopnoea, Poor chest excursion
• Distended, tympanic abdomen, absent bowel sounds
• Hypotonia, reduced reflexes

Problems From Lab Data

• Hypokalaemia, Hypophosphataemia, Hypocalcaemia (7.94 corrected)
• Normocytic anaemia
• Leucocytosis
• Elevated CK
• AST, ALT and Bilirubin elevated
• Urine - evidence of bacterial infection

Problems from radiology

• Raised Right hemi-diaphragm
• Distended loops of bowel; no mass lesion.

Assessment

1) First of all, we need to consider why this patient has developed vomiting and diarrhoea. Is it related to an infectious agent or related to a mechanical problem or even drug related? The problem appears to have started after taking a new PD drug. It is certainly possible that a drug side effect could have caused these symptoms. However, the patient stopped the drug but the symptoms persisted making the drug, whatever it is, less likely to be the cause of the problem.

The fact that the patient was taking senna and causing up to 6 episodes of diarrhoea a day is a concern. Normally, senna might cause 1 or two stools per day and therefore if copious diarrhoea is occurring, it is either over use of senna or a different pathology entirely.

Drugs known to slow the activity of the bowel include tricyclic antidepressants due to their anti-cholinergic effects and Aricept for similar reasons. Hence, they might result in a constipation-type of problem with over flow diarrhoea then occurring. However, in this case, there was no evidence of constipation on abdominal Xray which suggests that constipation was not a current problem.

Parkinson's disease can also result in constipation due to autonomic dysfunction and this is more profound in Multi-System Atrophy. Again, however, there was no evidence of constipation making the PD unlikely to be causing this problem.

In view of the high white cell count, and the dilated bowel one must consider several other diagnoses including clostridium difficile infection and inflammatory bowel disease (particularly ulcerative colitis). The former problem is a real possibility but in view of the lack of colonic haemorrhage, UC is unlikely here. Of course, a subacute mechanical obstruction might be due to an internal hernia or a malrotation of the bowel causing a volvulus.

The fact that the patient had a urinary tract infection identified is very important. This could be the cause of persistent vomiting and the leucocytosis. Moreover, UTI is a known cause of acute pseudo-obstruction of the bowel. This problem can result in electrolyte loss, vomiting, diarrhoea and constipation as well!

We must also consider why an ileus developed. Well, any of the above could result in an ileus. However, in view of the severe hypokalaemia, hypophosphataemia, it is entirely consistent that severe electrolyte depletion caused this problem although mechanical and infective causes would need to be ruled out first.

2) Then we should assess why the patient developed a reduced conscious level. Well a combination of hypovolaemia, infection, electrolyte disturbance and raised CO2 (hypercapnea) can all contribute to such a problem.

The fact that the respiratory rate dropped to 8 per minute with poor excursion of the chest in addition to skeletal muscle hypotonia and absent reflexes suggest diffuse muscle weakness. This would in turn result in respiratory failure with rising CO2 levels despite normal lungs, CO2 narcosis and unconsciousness. The muscle weakness could result from the profound hypokalaemia, hypophosphataemia and hypocalcaemia. Respiration would also be made worse by splinting the diaphragm with distended bowel.

3) Then we should assess why the patient had a bradycardia and a cardiac arrest. Well, this is multifactorial. Electrolyte disturbance e.g low K, Low Ca, can promote dysrhythmias. Hypovolaemia that this patient also experienced can cause cardiac arrest. These come from the 6 H's and 6 T's which are Reversible Causes.

H's

1. Hypothermia
2. Hyperkalaemia/hypokalaemia/electrolyte disturbance
3. Hypovolaemia
4. Hypoxia
5. Hypoglycaemia/Hyperglycaemia
6. Hydrogen ions (acidosis)

T's

1. Thromboembolism (PE)
2. Thrombosis (AMI)
3. Tension pneumothorax
4. Tamponade
5. Toxicity
6. Trauma

Moreover, one of the commonest causes of a a cardiac arrest is AMI which results from a dysrhythmia e.g. VT/VF, and should be ruled out in every patient.

4) Next we need to understand why the patient developed such severe electrolyte imbalance. Well, with a chronic history of recurrent vomiting and diarrhoea, various electrolytes can be lost. Loss of H+ ions from the stomach will cause metabolic alkalosis (and hypochloraemia) and diarrhoea can cause hypokalaemia. One should also remember that electrolytes can be lost in the urine, and so these should also be tested.

The loss of H+ ions causes the kidneys to have increased loss of K+ ions to maintain electroneutrality, and so these spill out into the urine resulting in worsening hypokalaemia! The proportional increased reuptake of bicarbonate over protons results in the metabolic alkalosis.

Thus, the arterial blood gas shows an acute respiratory acidosis (related to the CO2 retention) and a chronic metabolic alkalosis.

5) In view that the CK was raised, an MI should be ruled out and an ECG and Troponin T should be performed. In this case, the TropT was negative and the ECG revealed ST depression, T wave inversion and a prominent U wave all consistent with hypokalaemia. In view that an MI was excluded here, the cause of the CK rise could have been due to hypokalaemia associated Rhabdomyolysis or due to chest compression from the Cardiopulmonary rescuscitation.

In order to consider the kidneys, a urinary myoglobin level would be necessary. However, in such cases of renal failure following rhabdomyolysis, the CK is usually very high (several thousands) to result in renal impairment.

SUMMARY OF ANSWERS TO QUESTIONS

1) Why did the patient develop CO2 retention?

• Muscle weakness from combined Hypokalaemia, Hypophosphataemia , Hypocalcaemia
• Splitting of the diaphragm

2) Which two simple cardiac tests would you perform and why?

• ECG and Troponin T to look for dysrhythmias and rule out an MI.

3) Identify as many possible reasons why this patient developed a cardiac arrest?

• Multiple electrolyte disturbances particularly hypokalemia.
• Hypovolaemia
• Acidosis
  
• Possible AMI.

4) Which one urine test would you perform to investigate the cause of the possible renal failure in a patient with this clinical history?

• Urinary myoglobin level

5) Taking into account the entire history, list as many causes as possible for this patient developing an ileus. Is there a Syndrome that encompasses all of these features??

• Mechanical cause
• Infective Cause
• Inflammatory Cause
• Neoplastic (mass lesion; not seen on CT scan though)
• Electrolyte Imbalance
• Drugs
• Parkinson's disease

• Syndrome of Acute Pseudo-Obstruction is known as Ogilvie's Syndrome.

6) What does the arterial blood gas show and why do you think it occurred?

• Acute respiratory acidosis and a chronic metabolic acidosis.
• Acute changes due to respiratory failure from muscle weakness and reduced consciousness, chronic changes due to electrolyte loss resulting in raised level of HCO3.

• The liver function here was also abnormal- however with fluid and antibiotics, the levels improved quickly and may have resulted from sepsis, hepatic hypoperfusion amongst several causes.
• The chronic normocytic anaemia is also a problem here and a haematinics work up, blood smear and autoimmune profile to exclude autoimmune haemolysis (raised bilirubin and AST) plus a reticulocyte count would be warranted.

In this case, the patient was treated with intravenous K at a rate of 20mmol/hour as a continuous intravenous infusion plus a phosphate infusion whilst on an HCU being cardiac monitored. He was provided with 3 litres of intravenous fluid per day.

The patient was reviewed by the surgeons who agreed that this was indeed an acute pseudo-obstruction (Ogilvie's Syndrome) and a flatus tube was passed per rectum to reduce the bowel distension. Over several days, the distension decreased and bowel sounds could be heard suggesting bowel recovery. This was aided by the use of intravenous Erythromycin which has evidence to cause increased bowel motility.

The ECG returned to normal.

The patient was able to breath by himself without the aid of assisted non-invasive ventilation. The Blood gas also began to reverse towards normal.

However, the patient developed a polyuria of up to 6 litres per day. The serum osmolality was normal and the urine osmolality was dilute at about 380 mOsm/L. The patient still required large amounts of fluid daily to maintain his blood pressure in addition to dopamine catecholamine support.

During the illness, the patient revealed no evidence of renal failure, in part, because aggressive fluid management was commenced on admission to maintain renal perfusion. Therefore, this makes an acute tubular necrosis unlikely. Moreover, the patient did not have any profound oliguria or anuria suggestive of renal failure.

The polyuria suggested an insensitivity to ADH (nephrogenic diabetes insipidus) which can be caused by---- hypokalaemia !!! Patients who are well and who have polyuria and polydipsia can usually undergo a water deprivation test once diabetes mellitus has been excluded. However, in view that this patient was bed-bound and reliant on intravenous fluid to maintain blood pressure in addition to catecholamine support, it was considered unsafe to perform such a test. Therefore, an ADH level was attained which showed a mildly elevated level. In view that most causes of nephrogenic DI result in a partial insensitivity to ADH rather than a complete insensitivity, the use of supraphysiological doses of ADH (e.g. nasal desmopressin) can sometimes reverse such problems.


There are many causes of nephrogenic DI including congenital and acquired. These include:

• sickle cell disease
• medullary sponge kidney
• release of periureteral fibrosis
• pyelonephritis
• hypokalaemia
• hypercalcaemia
• amyloidosis
• Sjogren's syndrome
• myeloma
• lithium
• demeclocycline (used to treat SIADH)

Another potential cause was Fanconi Syndrome which in some patients is related to chronic hypokalaemia, the treatment of which is fluid replacement until there is spontaneous recovery of the kidneys.

So, this case was extremely complex related mostly to electrolyte disturbance!!

I hope that you enjoyed the case!

Please let me know your comments.

Have a great weekend!!