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Renal papillary necrosis

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Renal papillary necrosis is selective tissue death of the renal papilla causing a nephropathy. 

Presentation may be with loin pain and haematuria. It can cause both acute and chronic renal failure. 

Causes: 
  • Most common: 
    • Analgesic overuse
    • Urinary tract obstruction 
    • Diabetes 
    • Sickle cell 
  • Other: 

Pyelonephritis is often listed as a cause but this is controversial – it is difficult to determine if it is in fact a cause or an effect. 

Investigation is with IVU or CT. 
Urine may show a sterile pyuria.


References:

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Subarachnoid haemorrhage

Subarachnoid haemorrhage is bleeding into the space between the subarachnoid membrane and the pia mater.

It accounts for 5-10% of all strokes.
Incidence is 8-10 cases per 100 000 per year.
It is most frequent in those aged 55 to 60.
SAH accounts for 3% of patients presenting to ED with headache.

Classical presentation is a thunderclap occipital headache - "as if kicked in head"-  with vomiting and neck stiffness.
Sentinel headache is now seen as less relevant.

Causes of SAH:
  • ruptured berry aneurysm (75%)
  • malformations (5%)
  • idiopathic
  • (post trauma)

Common sites of berry aneurysms are:
  • junction of the posterior communicating artery with the internal carotid
  • junction of the anterior communicating artery with the anterior cerebral artery
  • the bifurcation of the middle cerebral artery

20% of berry aneurysms are multiple.
Subarachnoid haemorrhages are associated with:

Investigation is:
  • CT - >90% of bleeds detected within 24 hrs; sensitivity declines rapidly after 10 days
  • LP - done >12hrs after onset looking for xanthochromia. If the analysis of fluid will be delayed the sample should be protected from light to prevent degradation of bilirubin

Management:
  • neurosurgical referral – coiling is now replacing clipping as the treatment of choice
  • prompt angiography if surgery likely
  • nimodipine
  • possibly hyperventilation – cerebral vasculature reacts to arterial CO2 tension so lower CO2 would lower ICP

Outcome:
  • 30 day mortality rate of 45%
  • Predictors of mortality are age, decreased GCS on admission and large volume of blood on initial CT
  • a third of survivors moderately to severely disabled
  • most re-bleeds occur in the first 3 weeks

Complications:
  • rebleeding
  • hydrocephalus – 20%
  • cardiac dysfunction
  • hyponatraemia – 30%
  • hypomagnesaemia – associated with poor outcome; consider replacement if <0.7mmol

Small print gem: ECG abnormalities are common and troponin is raised in up to 30% of cases. It is thought this is because of excessive myocardial catecholamine release, caused by the SAH.

References:

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Erythema ab igne

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Erythema ab igne is a reticular, reddish discoloration of the skin caused by repetitive, prolonged heat exposure.

Classically it was caused by sitting near radiators or using hot water bottles against skin to relieve pain.  In modern times laptop computers have been a cause.

Note the similarity in appearance to livedo reticularis.


References:

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Legionella

/ / / / /
Legionella are gram negative bacilli. They are intracellular organisms.

Legionella bacteria cause 2 distinct clinical conditions: 
  1. Legionnaires disease, a severe multisystem disease which includes pneumonia 
  2. Pontiac fever, a self-limiting flu-like illness without pneumonia 

The natural environment for legionella is water, and they multiple at temperatures between 25 and 42C, with 35C being their optimal temperature meaning that hot water systems, whirlpools etc are ideal breeding grounds. Many outbreaks have also been associated with air-conditioning systems or with travel, especially cruise ships. 

Symptoms of Legionnaire disease include 
  • Fever 
  • Dry cough 
  • Dyspneoa 
  • Nausea, vomiting and abdominal pain 
  • Confusion 
The incubation period is 2 to 18 days.

Legionnaire disease is also associated with 
  • Hyponatraemia 
  • Deranged LFTs 
  • Thrombocytopeaenia 

Diagnosis may be by 
  • Urinary antigen 
  • Sputum culture 
  • Serology 

Most patients have abnormal CXR at presentation, most commonly patchy basal consolidation. Up to 30% have pleural effusions. 

Treatment is with antibiotics with a high intracellular concenration, such as azithromycin, clarithromycin, fluroquinolone or rifampacin.  Note that Legionnaires disease is a notifiable disease.


References:

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Livedo reticularis

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Livedo reticularis is a mottled, recticulated red-purple discoloration of the skin. 

Causes include:

Note the similarity in appearance between livedo reticularis and erythema ab igne. 


References:

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Syphilis

/ / / /
Syphilis is a sexually transmitted disease caused by the spirochaete treponema pallidum. 

Stages of syphilis can be divided into: 

Primary syphilis
  • Incubation 2-3 weeks 
  • Painless ulcer known as a chancre 
  • Often local, non-tender lymphadenopathy 

Secondary syphilis
  • Incubation 6 -12 weeks 
  • Systemic infection – malaise, rash, generalized lymphadenopathy 
  • Possibly wart-like lesions called condylomata lata 
 
Latent syphilis 
Subdivided into asymptomatic syphilis of less than 2 years duration (= early latent) or asymptomatic syphilis of more than 2 years duration (=late latent)

Tertiary syphilis
  • Neurosyphilis 
    • Tabes dorsalis 
      • Ataxia 
      • Lightning pains 
      • Argyll-Robertson pupils 
      • Absent limb reflexes 
      • Dorsal column signs (loss of vibration and proprioception) 
      • Romberg’s sign 
    • General paralysis of the insane 
      • Personality changes
      • Confusion
      • Seizures 
  • Cardiovascular syphilis 
    • Aortic aneursym 
    • Aortic regurgitation 

Diagnosis 
  • Dark ground microscopy for T pallidum in specialist centres 
  • T pallidum assays – tend to be positive lifelong, even after treatment 
  • Venereal Disease Reference Laboratory (VDRL) 
    • Not syphilis specific 
    • False positives in viral infections (chicken pox, hepatitis, infectious mononucleosis, malaria, HIV), SLE, RA, psoriasis 

Treatment
IM penicillin or PO doxycycline 



Small print gem: Jarisch-Herxheimer reaction – fever, myalgia and arthralgia hours after starting treatment for syphilis due to the rapid death of treponemes. 


References:

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Gynaecomastia

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Gynaecomastia is the benign enlargment of male breast tissue.  Male breast enlargement due to adipose is pseudogynaecomastia. 

Causes of gynaecomastia include 

Medications
  • Cardiac medications
    • spironolactone
    • eplerinone
    • amiodarone
    • digoxin
    • calcium channel blockers
  • Psychiatric medications
    • TCAs
    • risperidone
    • diazepam
  • Other
    • ketoconazole
    • metronidazole
    • finasteride
    • PPIs
    • cimetidine
    • phenytoin
    • steroids
    • chemotherapy drugs

Recreational drugs
  • marijuana
  • heroin
  • alcohol

Pathological

Physiological
  • newborns
  • adolescence 
  • old age (decreasing testosterone)

References:



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Marfan syndrome

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Marfan syndrome is an autosomal dominant disorder of fibrous connective tissue resulting in clinical manifestations in the skeletal, ocular and cardiovascular systems. 

Features of Marfan syndrome may include: 
  • Skeletal 
    • Increased height 
    • Reduced arm span to height ratio >1.05 
    • Scoliosis
    • Pectus carinatum or excavatum 
    • Joint hypermobility 
  • Occular 
    • Ectopia lentis
    • Myopia
  • Cardiovascular 
    • Aortic dilation 
    • Mitral valve prolapse 
  • Other 
    • Spontaneous pneumothorax 
    • Lumbrosacral dural ectasia

Classic Marfans is caused by a mutation in the gene FBN1 which encodes fibrillin-1. 

Diagnosis is by the extensive Ghent criteria. 

Management:
  • Beta blockers to slow rate of aortic aneurysm 
  • Surgery for aortic aneurysm once >5cm 
  • Avoidance of contact sports 


References:

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Ramsay-Hunt Syndrome

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Ramsay Hunt Syndrome is the reactivation of varicella zoster in the geniculate ganglion of the facial nerve.

It is characterised by:
  • herpes zoster oticus (=herpetic eruption in external auditory meatus)
  • facial nerve palsy
  • +/- deafness, tinnitus and vertigo
Treatment is with oral antivirals and prednisolone.

The prognosis is less good than for Bell’s Palsy – patients are less likely to make a full recovery.


Reference:

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Facial nerve palsy

/ / /
The facial nerve is the 7th cranial nerve. It has 5 major branches which may be recalled by “To Zansibar By Motor Car” = temporal, zygomatic, bucal, mandibular and cervical branches.

The functions of the facial nerve are:
  • Motor control of muscles of facial expression
  • Innervation of stapedius in ear
  • Supply of submandibular, parotid and sublingual glands
  • Efferent limb of corneal reflex
  • Taste sensation to anterior two-thirds of tongue

Unilateral facial nerve palsy

Unilateral facial nerve palsy is primary (idiopathic) in 75% of cases. It is then known as Bells Palsy.

Secondary facial nerve palsy is less common (25% of cases). 
Causes include:
  • diabetes
  • pontine infarct
  • infection – herpes simplex, varicella zoster (=Ramsey Hunt Syndrome), otitis media, syphilis
  • MS
  • Neurosarcoidosis
  • Tumour
  • Trauma
  • GBS
  • MG
  • Drugs – interferon, linezolid

Bells Palsy

Bell’s Palsy is characterised by:
  • Unilateral facial weakness
  • Pain behind the ear/aural fullness
  • Absent taste sensation to anterior two-thirds of tongue

Although Bell’s Palsy is ‘idiopathic’ it is hypothesised to be linked to viral infection.

Incidence is 20 per 100000
Peak onset is between 15 and 45 yrs of age
Both genders are equally affected

Management of Bells Palsy is:
  • Protect the eye from drying out
  • Steroids – prednisolone 1mg/kg
  • aciclovir

Prognosis is generally good – around 90% make a fully recovery, and 85% report some improvement in the first 3 weeks.



Bilateral facial nerve palsy
Consider GBS, diabetes, infection, neurosarcoidosis.

Small print gem: Some subsequently suffer from 'crocodile tears' = eating stimulates unilateral lacrimination instead of salivation.

References:

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Homocystinuria

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Homocystinuria is an autosomal recessive metabolic disorder which results in the accumulation of homocysteine due to decreased activity of cystathionine beta-synthase. 

Features of homocystinuria include: 
  • Myopia Ectopia lentis (=lens dislocation) 
  • Low IQ 
  • Marfanoid body habitus 
  • Thromboembotic events 
  • Osteoporosis 

Homocystinuria is also associated with malar flush and livedo reticularis. 

Diagnosis: 
  • Elevated plasma homocystine and methionine 
  • Elevated urinary homocystine 

Treatment: 
  • Methionine/protein-restricted diet 
  • Pyridoxine (vitamin B6; a cofactor for cystathionine beta-synthase ) 
    • Two types of homocystinuria exist – one responds well to pyridoxine, the other doesn’t 
  • Possibly B12/folate supplements – these encourage conversion of homocystine back to methionine. 

References:

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Disseminated intravascular coagulation

/ / /
Disseminated intravascular coagulation (DIC) is the pathological widespread activation of coagulation, resulting in thrombosis, haemorrhage or both.

Blood tests will show:
  • prolonged PT
  • prolonged aPTT
  • massively raised d-dimer levels
  • low platelets
  • low fibrinogen
  • schistocytes – around 50% of cases

Of these, it is the level of fibrinogen which best correlates to the severity – but note that as it is an acute phase protein it may initially be high so take time to become low.

Causes of DIC include:
  • obstetric – multiple, including placental abruption, HELLP
  • trauma – crush injury, burns, frostbite
  • septicaemia
  • malignancy
  • immune-mediated: transfusion reaction, severe allergic reaction, acute transplant rejection
  • toxins – bites, amphetamine overdose

The treatment is:
  • treat the cause
  • give platelets if platelets <50
  • cryoprecipitate – this replaces fibrinogen
  • FFP
  • activated protein C if septic.

References:

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Lambert-Eaton syndrome

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Lambert-Eaton syndrome is an autoimmune disorder characterised by:
  • Muscle weakness which improves on exercise 
  • Hyporeflexia or areflexia 
  • Autonomic dysfunction 

The commonest presenting symptom is leg weakness. Proximal muscles tend to be more affected than distal ones.

It is caused by IgG blocking voltage-gated calcium channels, preventing acetylcholine release.

For around 60% of patients with Lambert-Eaton it is a paraneoplastic syndrome and they have underlying small cell carcinoma of the lung (SCLC). However, the incidence of Lambert-Eaton in those with SCLC is around 3%. Other cancers rarely associated with Lambert-Eaton include breast, colon, bladder, kidney and prostate. It may also be an autoimmune condition with no underlying cancer.

Treatment is with 3,4-diaminopyridine which works by blocking voltage-gated potassium channels.

Since Lambert-Eaton Syndrome can precede presentation of SCLC regular CXR should be undertaken. The risk of developing SCLC becomes negligible 4 years after diagnosis of Lambert-Eaton.

Key points to differentiate between Myasthenia Gravis (MG) and Lambert-Eaton are:
  • Weakness gets worse on exercise with MG but improves with Lambert-Eaton
  • Reflexes are normal in MG but decreased/absent in Lambert-Eaton
  • There are not autonomic features in MG whilst there are in Lambert-Eaton


References:

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Lyme disease

/ / / /
Lyme disease is a tick-borne infectious disease caused by the gram negative spirochete borrelia burgdorferi. 

Clinical presentation is variable, but generally the first sign is erythema chronicum migrans, which is a spreading erythematous rash with central clearing. This is often accompanied by a flu-like illness. 

Complications associated with Lyme disease include:
  • Encephalitis 
  • Meningitis 
  • Arthritis 
  • Facial nerve palsy 
  • Meningoradiculitis 

In addition to erythema chronicum migrans two other skin manifestations are associated with Lyme disease: 
  • Borrelial lymphocytoma 
    • Usually occurs within 2 months of the tick bite 
    • is a purple tumour that appears on the earlobe, nipple, scrotum, nose or arms 
  • Acrodermatitis chronica atrophicans 
    • Occurs 6 months to several years after the tick bite 
    • Results in parchment-like thinning of skin, usually on extensor surfaces of limbs 

The diagnosis is often clinical. Screening for Lyme disease is done by ELISA and confirmation can be made by an immunoblot. 

CSF may show raised protein and lymphocytosis.

Treatment is 14 days doxycycline, or in more serious disease IV ceftriaxone. 


References:

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Klinefelter’s syndrome

/ / /
Klinefelter’s syndrome is a chromosomal disorder in which men have at least one extra X chromosome. The most common karyotype for Klinefelters is XXY

Characteristics of Klinefelter’s syndrome include:
  • Small testes
  • Gynaecomastia
  • Tall stature
  • Azoospermia
  • Sparse facial and body hair
  • Possibly learning difficulties

Blood tests show
  • Low testosterone
  • High LH/FSH

Around 1 in 500 men are affected, making it the most common disorder of sex chromosomes.

Associations:
  • increased risk of breast cancer
  • endocrine problems - diabetes, hypothyroidism
  • autoimmune conditions - SLE, RA
  • osteoporosis – 25%

Treatment: testosterone replacement therapy


References:

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Myasthenia gravis

/ / / /
Myasthenia gravis is a rare autoimmune disorder which causes fatigable muscle weakness.

Symptoms of myasthenia gravis (MG) vary from day to day but tend to be worse in the evening.

The most common muscles affected, in decreasing frequency, are:
  • Levator palpebrae superioris
  • Extraocular muscles
  • Proximal limb muscles
  • Muscles of facial expression
  • Neck extensors

Myasthenic crisis is worsening of myasthenia resulting in paralysis of respiratory muscles and the requirement for respiratory support. This is usually precipitated by infections or insufficient treatment.

Diagnosis
  • Electrodiagnostic – repetitive stimulation leads to decreased evoked response
  • Antibodies
    • acetylcholine receptor antibodies – present in 80%-90% of patients with generalised MG
    • MuSK antibodies - present in around 30%
  • the tensilon test = administration of edrophonium chloride causes an unequivocal improvement in strength

Note reflexes are normal or brisk in MG – in contrast, they are absent in Lambert Eaton syndrome,

Treatment
  • Acetylcholinesterase inhibitors
  • Prednisolone
  • Plasmaphoresis if crisis
  • IV IG if crisis
  • Thymectomy – up to 80% experience improvement

Drugs which should be avoided as they worsen MG include:
  • Penicillamine
  • Some antibiotics (aminoglycosides, macrolides, fluoroquinolones)
  • Beta blockers
  • Calcium channel blockers
  • Quinine
  • Phenytoin

Other factors which can worsen MG include:
  • Hot temperature
  • Emotion
  • Hyperthyroidism (note around 10% of patients with MG have hyperthyroidism)
  • Pregnancy
  • Hypokalaemia

References:

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Botulism

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Botulism is a disease caused by clostridium botulinum (gram positive bacillus) which results in a descending, symmetrical flaccid paralysis. This is caused by blocking acetylcholine release from the presynaptic membrane. 

The main causes of botulism are either via food (classically canned food) or by wound infection (most frequently in heroin users) 

Clinical features of botulism include: 
  • Cranial nerve palsies (the first sign) 
    • Blurred vision/diplopia 
    • Dsyarthria 
    • Ptosis 
  • Descending flaccid paralysis 
  • Respiratory arrest 

Sensory pathways are unaffected and intellectual function is preserved. 

Routine/’normal’ lab tests are not useful for diagnosis of botulism but can be helpful to rule out differential diagnosis. For example, CSF may be helpful to distinguish botulism from Guillain-Barre syndrome – CSF protein is normal in botulism but raised in Guillain-Barre syndrome. Additionally the tensilon test may also be useful to distinguish botulism from myasthenia gravis; however, borderline positive tensilon tests have occurred in cases of botulism. Confirmation of botulism can be achieved by confirming presence of the toxin. 

Treatment is with antitoxin and intensive care. 


References:

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Renal tubular acidosis

/ / /
Renal tubular acidosis describes a group of transport defects in the kidney affecting the reabsorption of bicarbonate, the excretion of hydrogen ions or both.

Renal tubular acidosis results in
  • Hyperchloraemia
  • Metabolic acidosis
  • Normal anion gap
  • Normal/only slightly reduced eGFR

Renal tubular acidosis (RTA) are divided into:

Type 1 = Distal RTA

This is due to impaired secretion of hydrogen ions in the form of NH4+.
It is the most common form.
It is often associated with hypokalaemia.

Causes include:

Diagnosis is by oral acid load with ammonium chloride - the urine should become more acid, but in type 1 RTA the pH remains >5.5. 

Treatment: oral bicarbonate, possibly thiazide diuretic.


Type 2 = Proximal RTA

Type 2 RTA is due to impaired bicarbonate reabsoption in the proximal tubule.

Causes include:

Diagnosis is by IV bicarbonate loading - normally fractional excretion is <5% of the filtered load, but in type 2 RTA it is around 15%.

Treatment: oral bicarbonate.


Type 3 RTA = a combination of type 1 and type 2


Type 4 RTA = Hyperkalaemic RTA 

This is caused by hyperkalaemia impairing NH4+ formation

Causes are therefore any cause of hyperkalaemia, such as Addison’s or drug induced hyperkalaemia.

Treatment is to treat cause and control hyperkalaemia


References:

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Notifiable diseases

Notifiable diseases are infectious diseases which doctors have a statutory duty to report to the 'Proper officer' of their local authority.  Reports should be made within 3 days or verbally within 24 hours if the case is serious.  Doctors should not wait for laboratory confirmation before making a report.

The list of notifiable diseases on the HPA website as of October 2011 is:
  • Acute encephalitis 
  • Acute meningitis 
  • Acute poliomyelitis 
  • Acute infectious hepatitis 
  • Anthrax 
  • Botulism 
  • Brucellosis 
  • Cholera 
  • Diphtheria 
  • Enteric fever (typhoid or parathyohoid fever) 
  • Food poisoning 
  • Haemolytic uraemic syndrome 
  • Infectious bloody diarrhoea 
  • Invasive group A streptococcal disease and scarlet fever
  • Legionnaire’s Disease 
  • Leprosy 
  • Malaria 
  • Measles 
  • Meningococcal septicaemia 
  • Mumps 
  • Plague 
  • Rabies 
  • Rubella 
  • SARS 
  • Smallpox 
  • Tetanus 
  • Tuberculosis 
  • Typhus 
  • Viral haemorrhagic fever 
  • Whooping cough 
  • Yellow fever 

Reference:

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Multiple myeloma

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Mutiple myeloma is a malignant monoclonal proliferation of plasma cells.
The commonest subclass is IgG (IgG>IgA>IgM)

Incidence is 4 per 100000
Commonest in those in their 70s
Males > females (1.5:1)
Twice as common in those of Afro-Caribbeam descent compared to Caucasian.
Average survival 4 to 6 years
Higher beta 2 microglobulin implies a worse prognosis.

Symptoms:
  • osteolytic bone lesions --> backache/pathological fractures
  • fatigue due to anaemia
  • symptoms of hypercalcaemia
  • bacterial infections due to immunoparesis
  • renal impairment due to light chains
  • symptoms associated with hyperviscosity

However, over 30% of patients are asymptomatic when myeloma is detected.

Investigations:
  • Bloods:
    • normocytic normochromic anaemia
    • rouleaux on blood film
    • raised calcium (40%)
    • raised urea and creatinine
    • raised ESR
  • Urine
    • Bence Jones proteins (=free serum light chains) in urine (66%)
  • XR
    • ?pepper pot skull, vertebral collapse
  • bone marrow – 10% or more clonal bone marrow plasma cells

The diagnostic criteria for symptomatic myeloma is:
  • monoclonal protein band in serum or urine electrophoresis
  • increased plasma cells on BM biopsy
  • evidence of end organ damage from myeloma 
The diagnostic criteria for asymptomatic myeloma is:
  • monoclonal protein band in serum ≥30g/l a nd/or bone marrow clonal plasma cells ≥10%

Treatment:
  • supportive of complications
    • bisphosphonates to avoid fractures (Zoledronic acid is current preferred))
    • transfusions if severe anaemia
    • treatment of hypercalcaemia
  • chemotherapy:
    • younger (<65 yrs) or fit: VAD = vincristine, adriamycin (=doxorubicin), dexamethasone then ASCT (Autologous stem cell transplantation)
    • older: CDT or MDT = cyclophosphamide or melphalan with dexamethasone and thalidomide

Cylophosphamide and melphalan are alkylating agents.

Side effects of thalidomide include somnolence, neuropathy, deep venous thrombosis. Risk of DVT is much increased when combined with steroid treatment.

A new medication, Bortezomib, which is a new anticancer drug that works by reversible proteaseome inhibition. It is associated with thrombocytonia and peripheral neuropathy and is currently only recommended for patients who are not appropriate for aggressive therapy and do not tolerate thalidomide.

Complications of myeloma include:
  • Hyperviscosity syndrome
    • Hyperviscosity syndrome occurs most commonly in IgM myeloma (IgM>IgA>IgG)
    • Transfusions should be avoided in hyperviscosity syndrome.
  • hypercalcaemia
  • spinal cord compression - occurs in 5% at some point
  • acute renal failure - 20% at presentation, up to 50% at some point
    •  treat with at least 3 litres of normal saline daily
    • treat precipitating events eg hypercalcaemia, sepsis
    • high dose dexamethasone (unless CI) pending initiation of definitive treatment
  • AL amyloidosis (15%) 
  • VTE

Lasted reviewed March 2015

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Nail-patella syndrome

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Nail-patella syndrome is an autosomal dominant condition affecting 1 in 50 000. 

It is classically described as a tetrad of: 
  • Dysplasia of nails 
  • Small or absent patellae 
  • Elbow dysplasia 
  • Iliac horns – occur in 70%; pathognomonic. 

Other features associated with nail-patella syndrome are: 
  • Renal abnormalities (25%) 
  • Sometimes glaucoma in adulthood 


References:

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Brown-Sequard Syndrome

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Brown-Sequard Syndrome is a condition characterized by a lesion in the spinal cord resulting in:
  • Loss of motor function on ipsilateral side of the body below the level of the lesion (corticospinal tract compression)
  • Loss of proprioception and vibration sense (dorsal columns compression) below the level of the lesion ipsilaterally
  • Loss of pain and temperature sensation on other side of the body below the level of the lesion (spinothalamic tract compression)

Causes include:

Rare causes include:
  • Cervical disc herniation
  • After vaccination for diphtheria and tetanus
References:

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no
Secret collector of interesting anonymised ECGs. Fan of the Bath Photomarathon. Lover of cream teas. [Sarah Hudson] (Your Picture)