Moro's Health and Medicine Zone

European Hernia Society guidelines on the treatment of inguinal hernia in adult patients

Dr. Moro — Mon, 21 May 2012 19:32:51 +0000

Abstract

The European Hernia Society (EHS) is proud to present the EHS Guidelines for the Treatment of Inguinal Hernia in Adult Patients. The Guidelines contain recommendations for the treatment of inguinal hernia from diagnosis till aftercare. They have been developed by a Working Group consisting of expert surgeons with representatives of 14 country members of the EHS. They are evidence-based and, when necessary, a consensus was reached among all members. The Guidelines have been reviewed by a Steering Committee. Before finalisation, feedback from different national hernia societies was obtained. The Appraisal of Guidelines for REsearch and Evaluation (AGREE) instrument was used by the Cochrane Association to validate the Guidelines. The Guidelines can be used to adjust local protocols, for training purposes and quality control. They will be revised in 2012 in order to keep them updated. In between revisions, it is the intention of the Working Group to provide every year, during the EHS annual congress, a short update of new high-level evidence (randomised controlled trials [RCTs] and meta-analyses). Developing guidelines leads to questions that remain to be answered by specific research. Therefore, we provide recommendations for further research that can be performed to raise the level of evidence concerning certain aspects of inguinal hernia treatment. In addition, a short summary, specifically for the general practitioner, is given. In order to increase the practical use of the Guidelines by consultants and residents, more details on the most important surgical techniques, local infiltration anaesthesia and a patient information sheet is provided. The most important challenge now will be the implementation of the Guidelines in daily surgical practice. This remains an important task for the EHS. The establishment of an EHS school for teaching inguinal hernia repair surgical techniques, including tips and tricks from experts to overcome the learning curve (especially in endoscopic repair), will be the next step. Working together on this project was a great learning experience, and it was worthwhile and fun. Cultural differences between members were easily overcome by educating each other, respecting different views and always coming back to the principles of evidence-based medicine. The members of the Working Group would like to thank the EHS board for their support and especially Ethicon for sponsoring the many meetings that were needed to finalise such an ambitious project.

Guidelines for the treatment of inguinal hernia in adult patients committees

Steering Committee

Maarten Simons: Coordinator
Marc Miserez: EHS contact
Giampiero Campanelli
Henrik Kehlet
Andrew Kingsnorth
Par Nordin
Volker Schumpelick

Working Group

Austria:: Rene Fortelny
Belgium:: Marc Miserez
Denmark:: Morten Bay Nielsen
Finland:: Timo Heikkinen
France:: Jean-Luc Bouillot
Germany:: Joachim Conze
Hungary:: Georg Weber
Italy:: Giampiero Campanelli
Netherlands:: Theo Aufenacker/Maarten Simons
Poland:: Maciej Smietanski
Spain:: Salvador Morales-Conde
Sweden:: Sam Smedberg/Par Nordin
Switzerland:: Jan Kukleta
United Kingdom:: Andrew Kingsnorth

Reference Manager

Diederik de Lange (NL)

Summary of guidelines on inguinal hernia in adult patients (>18 years)

Anamnesis Groin swelling, right/left, nature of complaints (pain), duration of complaints, contralateral groin swelling, signs and symptoms of incarceration, reducibility, previous hernia operations.Predisposing factors: smoking, chronic obstructive pulmonary disease (COPD), abdominal aortic aneurysm, long-term heavy lifting work, positive family history, appendicectomy, prostatectomy, peritoneal dialysis.

Physical examination (Reducible) swelling groin (above the inguinal ligament), differentiation lateral/medial unreliable, operation scar inguinal region, contralateral groin, symptoms of incarceration, reducible, testes, ascites, rectal examination.

Differential diagnosis Swelling: Femoral hernia, incisional hernia, lymph gland enlargement, aneurysm, saphena varix, soft-tissue tumour, abscess, genital anomalies (ectopic testis).Pain: adductor tendinitis, pubic osteitis, hip artrosis, bursitis ileopectinea, irradiating low back pain.Women: consider femoral hernia, endometriosis.

Diagnostics Clinical investigation. If any (rarely necessary): ultrasound, magnetic resonance imaging (MRI) (with and without Valsalva manoeuvre), herniography.

Treatment Men with asymptomatic or minimally symptomatic inguinal hernia (without or only minimal complaints): consider conservative management.Incarcerated hernia (no strangulation symptoms): try reduction.Strangulated hernia: emergency surgery.Symptomatic inguinal hernia: elective surgery.Women: consider femoral hernia, consider preperitoneal (endoscopic) approach.

Operation technique (male adults)

Primary unilateral:: Mesh repair: Lichtenstein or endoscopic repair are recommended. Endoscopic repair only if expertise is available.
Primary bilateral:: Mesh repair: Committee’s recommendation: Lichtenstein or endoscopic.
Recurrent inguinal hernia:: Mesh repair: Committee’s recommendation: modify technique in relation to previous technique.
If previously anterior:: Consider open preperitoneal mesh or endoscopic approach (if expertise is present).
If previously posterior:: Consider anterior mesh (Lichtenstein).

Note 1: The Committee is of the opinion that a totally extraperitoneal (TEP) repair is preferred to a transabdominal preperitoneal (TAPP) approach in the case of endoscopic surgery.
Note 2: The Committee is of the opinion that, except for the Lichtenstein and endoscopic techniques, none of the alternative mesh techniques have received sufficient scientific evaluation to be given a place in these guidelines.

Prophylactic antibiotics: In open surgery, not recommended in low-risk patients. Not recommended in endoscopic surgery.
Anaesthesia: Most open (anterior) inguinal hernia techniques are eligible for local anaesthesia.
: Exclusion considerations: young anxious patients, morbid obesity, incarcerated hernia.
: Anterior: all forms of anaesthesia, consider local anaesthesia.
: Avoid spinal anaesthesia with high doses of long-acting anaesthetics.
: All patients should have long-acting local anaesthetic infiltration preoperatively for postoperative pain control.
Day surgery: ASA I and II: always consider day surgery.
: ASA III/IV: consider local anaesthesia, consider day surgery.

Flow diagram for the treatment of inguinal hernia in male adults

Based on a consensus within the Committee.

Fig. 1

(Oxford Centre for Evidence-Based Medicine)

Levels of evidence:

1A: Systematic review of randomised controlled trials (RCTs) with consistent results from individual (homogenous) studies.
1B: RCTs of good quality.
2A: Systematic review of cohort or case–control studies with consistent results from individual (homogenous) studies.
2B: RCT of poorer quality or cohort or case–control studies.
2C: Outcome studies, descriptive studies.
3: Cohort or case–control studies of low quality.
4: Expert opinion, generally accepted treatments.

Grades of recommendation:

A: Supported by systematic review and/or at least two RCTs of good quality.
: Level of evidence 1A, 1B.
B: Supported by good cohort studies and/or case–control studies.
: Level of evidence 2A, 2B.
C: Supported by case series, cohort studies of low quality and/or ‘outcomes’ research.
: Level of evidence 2C, 3.
D: Expert opinion, consensus committee.
: Level of evidence 4.

All conclusions and recommendations:

Indications for treatment

Conclusions

Level 1B: Watchful waiting is an acceptable option for men with minimally symptomatic or asymptomatic inguinal hernias.

Level 4: A strangulated inguinal hernia (with symptoms of strangulation and/or ileus) should be operated on urgently.

Recommendations

Grade A: It is recommended in minimally symptomatic or asymptomatic inguinal hernia in men to consider a watchful waiting strategy.

Grade D: It is recommended that strangulated hernias are operated on urgently.
: It is recommended that symptomatic inguinal hernias are treated surgically.

Non-surgical diagnostics

Conclusions

Level 2C: In case of an evident hernia, clinical examination suffices.
: Differentiation between direct and indirect hernia is not useful. Only cases of obscure pain and/or doubtful swelling in the groin require further diagnostic investigation.
: In everyday practice, the sensitivity and specificity of ultrasonography for diagnosing inguinal hernia is low.
: A computed tomography (CT) scan has a limited place in the diagnosis of an inguinal hernia.
: MRI has a sensitivity and specificity of more than 94% and is also useful to reveal other musculo-tendineal pathologies.
: Herniography has high sensitivity and specificity in unclear diagnosis but has a low incidence of complications. It does not reveal lipomas of the cord.

Recommendations

Grade C

It is recommended that groin diagnostic investigations are performed only in patients with obscure pain and/or swelling.

The flow chart recommended in these cases:

Ultrasound (if expertise is available)
If ultrasound negative → MRI (with Valsalva)
If MRI negative → consider herniography

Classification

Recommendations

Grade D: It is recommended that the EHS classification for hernia in the groin is used.

Risk factors and prevention

Conclusions

Level 3: Smokers, patients with positive family hernia history, patent processus vaginalis, collagen disease, patients with an abdominal aortic aneurysm, after an appendicectomy and prostatectomy, with ascites, on peritoneal dialysis, after long-term heavy work or with COPD have an increased risk of inguinal hernia. This is not proven with respect to (occasional) lifting, constipation and prostatism.

Recommendations

Grade C: Smoking cessation is the only sensible advice that can be given with respect to preventing the development of an inguinal hernia.

Treatment of inguinal hernia

Conclusions

Level 1A: Operation techniques using mesh result in fewer recurrences than techniques which do not use mesh.
: The Shouldice hernia repair technique is the best non-mesh repair method.
: Endoscopic inguinal hernia techniques result in a lower incidence of wound infection, haematoma formation and an earlier return to normal activities or work than the Lichtenstein technique.
: Endoscopic inguinal hernia techniques result in a longer operation time and a higher incidence of seroma than the Lichtenstein technique.

Level 1B: Mesh repair appears to reduce the chance of chronic pain rather than increase it. Endoscopic mesh techniques result in a lower chance of chronic pain/numbness than the Lichtenstein technique. In the long term (more than 3 to 4 years follow-up), these differences (non-mesh-endoscopic-Lichtenstein) seem to decrease for the aspect pain but not for numbness.
: For recurrent hernias after conventional open repair, endoscopic inguinal hernia techniques result in less postoperative pain and faster reconvalescence than the Lichtenstein technique.
: Material-reduced meshes have some advantages with respect to long-term discomfort and foreign-body sensation in open hernia repair, but are possibly associated with an increased risk for hernia recurrence (possibly due to inadequate fixation and/or overlap) (Chap. 2.9).
: From the perspective of the hospital, an open mesh procedure is the most cost-effective operation in primary unilateral hernias. From a socio-economic perspective, an endoscopic procedure is probably the most cost-effective approach for patients who participate in the labour market, especially for bilateral hernias. In cost–utility analyses including quality of life (QALYs), endoscopic techniques (TEP) may be preferable since they cause less numbness and chronic pain (Chap. 2.18).

Level 2A: For endoscopic inguinal hernia techniques, TAPP seems to be associated with higher rates of port-site hernias and visceral injuries, whilst there appear to be more conversions with TEP.

Level 2B: There appears to be a higher rate of rare but serious complications with endoscopic repair, especially during the learning curve period.
: Other open mesh techniques: Prolene hernia system (PHS), Kugel patch, plug and patch (mesh plug) and Hertra mesh (Trabucco), in short-term follow-up, result in comparable outcome (recurrence) to the Lichtenstein technique.
: A young man (aged 18–30 years) with a lateral inguinal hernia has a risk of recurrence of at least 5% following a non-mesh operation and a long follow-up (>5 years) (Chap. 2.8).

Level 2C: Endoscopic inguinal hernia techniques with a small mesh (≤8 × 12 cm) result in a higher incidence of recurrence compared with the Lichtenstein technique.
: Women have a higher risk of recurrence (inguinal or femoral) than men following an open inguinal hernia operation due to a higher occurrence of femoral hernias (Chap. 2.7).
: The learning curve for performing endoscopic inguinal hernia repair (especially TEP) is longer than that for open Lichtenstein repair, and ranges between 50 and 100 procedures, with the first 30–50 being most critical (Chap. 2.12).
: For endoscopic techniques, adequate patient selection and training might minimise the risks for infrequent but serious complications in the learning curve (Chap. 2.12).
: There does not seem to be a negative effect on outcome when operated by a resident versus an attending surgeon (Chap. 2.12).
: Specialist centres seem to perform better than general surgical units, especially for endoscopic repairs (Chap. 2.12).

Level 4: All techniques (especially endoscopic techniques) have a learning curve that is underestimated.
: For large scrotal (irreducible) inguinal hernias, after major lower abdominal surgery, and when no general anaesthesia is possible, the Lichtenstein repair is the preferred surgical technique.
: For recurrent hernias, after previous posterior approach, an open anterior approach seems to have clear advantages, since another plane of dissection and mesh implantation is used.
: Stoppa repair is still the treatment of choice in case of complex hernias.

Recommendations

Grade A: All male adult (>30 years) patients with a symptomatic inguinal hernia should be operated on using a mesh technique.
: When considering a non-mesh repair, the Shouldice technique should be used.
: The open Lichtenstein and endoscopic inguinal hernia techniques are recommended as the best evidence-based options for the repair of a primary unilateral hernia, providing the surgeon is sufficiently experienced in the specific procedure.
: For the repair of recurrent hernias after conventional open repair, endoscopic inguinal hernia techniques are recommended.
: When only considering chronic pain, endoscopic surgery is superior to open mesh.
Grade A: In inguinal hernia tension-free repair, synthetic non-absorbable flat meshes (or composite meshes with a non-absorbable component) should be used (Chap. 2.9).
: The use of lightweight/material-reduced/large-pore (>1,000-μm) meshes can be considered in open inguinal hernia repair to decrease long-term discomfort but possibly at the cost of increased recurrence rate (possibly due to inadequate fixation and/or overlap) (Chap. 2.9).
: It is recommended that an endoscopic technique is considered if a quick postoperative recovery is particularly important (Chap. 2.14).
: It is recommended that, from a hospital perspective, an open mesh procedure is used for the treatment of inguinal hernia (Chap. 2.18).
: From a socio-economic perspective, an endoscopic procedure is proposed for the active working population, especially for bilateral hernias (Chap. 2.18).

Grade B: Other open-mesh techniques than Lichtenstein (PHS, Kugel patch, plug and patch [mesh-plug] and Hertra mesh [Trabucco]) can be considered as an alternative treatment for open inguinal hernia repair, although only short-term results (recurrence) are available.
: It is recommended that an extraperitoneal approach (TEP) is used for endoscopic inguinal hernia operations.
: It is recommended that a mesh technique is used for inguinal hernia correction in young men (aged 18–30 years and irrespective of the type of inguinal hernia) (Chap. 2.8).

Grade C: (Endoscopic) hernia training with adequate mentoring should be started with junior residents (Chap. 2.12).

Grade D: For large scrotal (irreducible) inguinal hernias, after major lower abdominal surgery, and when no general anaesthesia is possible, the Lichtenstein repair is the preferred surgical technique.
: In endoscopic repair, a mesh of at least 10 × 15 cm should be considered.
: It is recommended that an anterior approach is used in the case of a recurrent inguinal hernia which was treated with a posterior approach.
: In female patients, the existence of a femoral hernia should be excluded in all cases of a hernia in the groin (Chap. 2.7).
: A preperitoneal (endoscopic) approach should be considered in female hernia repair (Chap. 2.7).
: All surgeons graduating as general surgeons should have a profound knowledge of the anterior and posterior preperitoneal anatomy of the inguinal region (Chap. 2.12).
: Complex inguinal hernia surgery (multiple recurrences, chronic pain, mesh infection) should be performed by a hernia specialist (Chap. 2.12).

Inguinal hernia in women

Conclusions

Level 2C: Women have a higher risk of recurrence (inguinal or femoral) than men following an open inguinal hernia operation due to a higher occurrence of femoral hernias.

Recommendations

Grade D: In female patients, the existence of a femoral hernia should be excluded in all cases of a hernia in the groin.
: A preperitoneal (endoscopic) approach should be considered in female hernia repair.

Lateral inguinal hernia in young men (aged 18–30 years)

Conclusions

Level 2B: A young man (aged 18–30 years) with a lateral inguinal hernia has a risk of recurrence of at least 5% following a non-mesh operation and a long follow-up (>5 years).

Recommendations

Grade B: It is recommended that a mesh technique is used for inguinal hernia correction in young men (aged 18–30 years and irrespective of the type of inguinal hernia).

Biomaterials

Conclusions

Level 1A: Operation techniques using mesh result in fewer recurrences than techniques which do not use mesh.

Level 1B: Material-reduced meshes have some advantages with respect to long-term discomfort and foreign-body sensation in open hernia repair, but are possibly associated with an increased risk for hernia recurrence (possibly due to inadequate fixation and/or overlap).

Recommendations

Grade A: In inguinal hernia tension-free repair, synthetic non-absorbable flat meshes (or composite meshes with a non-absorbable component) should be used.
: The use of lightweight/material-reduced/large-pore (>1,000-μm) meshes in open inguinal hernia repair can be considered to decrease long-term discomfort, but possibly at the cost of increased recurrence rate (possibly due to inadequate fixation and/or overlap).

Day surgery

Conclusions

Level 2B: Inguinal hernia surgery as day surgery is as safe and effective as that in an inpatient setting, and more cost-effective.

Level 3: Inguinal hernia surgery can easily be performed as day surgery, irrespective of the technique used.
: Selected older and ASA III/IV patients are also eligible for day surgery.

Recommendations

Grade B: An operation in day surgery should be considered for every patient.

Antibiotic prophylaxis

Conclusions

Level 1A: In conventional hernia repair (non-mesh), antibiotic prophylaxis does not significantly reduce the number of wound infections. NNT 68.

Level 1B: In open mesh repair in low-risk patients, antibiotic prophylaxis does not significantly reduce the number of wound infections. NNT 80
: For deep infections, the NNT is 352.

Level 2B: In endoscopic repair, antibiotic prophylaxis does not significantly reduce the number of wound infections. NNT ∞.

Recommendations

Grade A: In clinical settings with low rates (<5%) of wound infection, there is no indication for the routine use of antibiotic prophylaxis in elective open groin hernia repair in low-risk patients.

Grade B: In endoscopic hernia repair, antibiotic prophylaxis is probably not indicated.

Grade C: In the presence of risk factors for wound infection based on patient (recurrence, advanced age, immunosuppressive conditions) or surgical (expected long operating times, use of drains) factors, the use of antibiotic prophylaxis should be considered.

Training

Conclusions

Level 2C: The learning curve for performing endoscopic inguinal hernia repair (especially TEP) is longer than for open Lichtenstein repair, and ranges between 50 and 100 procedures, with the first 30–50 being the most critical.
: For endoscopic techniques, adequate patient selection and training might minimise the risks for infrequent but serious complications in the learning curve.
: There does not seem to be a negative effect on outcome when operated by a resident versus an attending surgeon.
: Specialist centres seem to perform better than general surgical units, especially for endoscopic repairs.

Recommendations

Grade C: (Endoscopic) hernia training with adequate mentoring should be started with junior residents.

Grade D: All surgeons graduating as general surgeons should have a profound knowledge of the anterior and posterior preperitoneal anatomy of the inguinal region.
: Complex inguinal hernia surgery (multiple recurrences, chronic pain, mesh infection) should be performed by a hernia specialist.

Anaesthesia

Conclusions

Level 1B: Open anterior inguinal hernia techniques can be satisfactorily performed under local anaesthetic.
: Regional anaesthesia, especially when using high-dose and/or long-acting agents, has no documented benefits in open inguinal hernia repair and increases the risk of urinary retention.

Recommendations

Grade A: It is recommended that, in the case of an open repair, local anaesthetic is considered for all adult patients with a primary reducible unilateral inguinal hernia.

Grade B: Use of spinal anaesthesia, especially using high-dose and/or long-acting anaesthetic agents, should be avoided.
: General anaesthesia with short-acting agents and combined with local infiltration anaesthesia may be a valid alternative to local anaesthesia.

Postoperative recovery

Conclusions

Level 1A: Endoscopic inguinal hernia techniques result in an earlier return to normal activities or work than the Lichtenstein technique.

Recommendations

Grade A: It is recommended that an endoscopic technique is considered if a quick postoperative recovery is particularly important.

Aftercare

Conclusions

Level 3: The imposition of a temporary ban on lifting, participating in sports or working after inguinal hernia surgery is not necessary. Probably a limitation on heavy weight lifting for 2–3 weeks is enough.

Recommendations

Grade C: It is recommended that limitations are not placed on patients following an inguinal hernia operation and patients are, therefore, free to resume activities. “Do what you feel you can do.” Probably a limitation on heavy weight lifting for 2–3 weeks is enough.

Postoperative pain control

Conclusions

Level 1B: Wound infiltration with a local anaesthetic results in less postoperative pain following inguinal hernia surgery.

Recommendations

Grade A: Local infiltration of the wound after hernia repair provides extra pain control and limits the use of analgesics.

Complications

Recommendations

Grade B: It is recommended in the case of open surgery to operatively evacuate a haematoma which results in tension on the skin.
: It is recommended that wound drains are only used where indicated (much blood loss, coagulopathies).

Grade C: It is recommended that seromas are not aspirated.

Grade D: It is recommended that the patient empties his/her bladder prior to endoscopic and open operations.
: It is recommended that the fascia transversalis/peritoneum is opened with restrictivity in open surgery of direct hernias. Take care that the bladder might be herniated.

Grade D: It is recommended that, in the case of large hernia sacs, transection of the hernia sac is performed and the distal hernia sac is left undisturbed, so as to prevent ischaemic orchitis. Damage to the spermatic cord structures should be avoided.

Grade D: It is recommended that patients with previous major lower (open) abdominal intervention or previous radiotherapy of pelvic organs do not undergo endoscopic inguinal hernia surgery.

Grade D: It is recommended that, due to the risk of intestinal adhesion and the risk of bowel obstruction, the extraperitoneal approach (TEP) is used for endoscopic inguinal hernia operations.
: It is recommended that trocar openings of 10 mm or larger are closed.

Grade D: It is recommended that the first trocar at endoscopic hernia surgery (TAPP) is introduced by the open technique.

Chronic pain

Conclusions; causes and risk factors

Level 1B: The risk of chronic pain after hernia repair with mesh is less than after non-mesh repair.
: The risk of chronic pain after endoscopic hernia repair is lower than after open hernia repair.

Level 2A: The overall incidence of moderate to severe chronic pain after hernia surgery is around 10–12%.
: The risk of chronic pain after hernia surgery decreases with age.

Level 2B: Preoperative pain may increase the risk of developing chronic pain after hernia surgery.
: Preoperative chronic pain conditions correlate with the development of chronic pain after hernia surgery.
: Severe early postoperative pain after hernia surgery is correlated to the development of chronic pain.
: Females have an increased risk of developing chronic pain after hernia surgery.

Conclusions; prevention of chronic pain

Level 1B: Material-reduced meshes have some advantages with respect to long-term discomfort and foreign-body sensation in open hernia repair (when only considering chronic pain).

Level 2A: Prophylactic resection of the ilioinguinal nerve does not reduce the risk of chronic pain after hernia surgery.

Level 2B: Identification of all inguinal nerves during open hernia surgery may reduce the risk of nerve damage and postoperative chronic groin pain.

Conclusions; treatment of chronic pain

Level 3: A multidisciplinary approach at a pain clinic is an option for the treatment of chronic post-herniorrhaphy pain.
: Surgical treatment of specific causes of chronic post-herniorrhaphy pain can be beneficial for the patient, such as the resection of entrapped nerves, mesh removal in mesh-related pain, removal of endoscopic staples or fixating sutures.

Recommendations

Grade A: The use of lightweight/material-reduced/large-pore (>1,000-μm) meshes in open inguinal hernia repair can be considered to decrease long-term discomfort (when only considering chronic pain).
: Endoscopic surgery is superior to open mesh (when only considering chronic pain), if a dedicated team is available.

Grade B: It is recommended that risks of development of chronic postoperative pain are taken into account when the method of hernia repair is decided upon.
: It is recommended that inguinal nerves at risk (three nerves) are identified at open hernia surgery.

Grade C: It is recommended that a multidisciplinary approach is considered for the treatment of chronic pain after hernia repair.
: It is recommended that the surgical treatment of chronic post-herniorrhaphy pain as a routine is restricted in the lack of scientific studies evaluating the outcome of different treatment modalities.

Mortality

Recommendations

Grade B: It is recommended to offer patients with femoral hernia early planned surgery, even if the symptoms are vague or absent.

Grade D: It is recommended to intensify efforts to improve the early diagnosis and treatment of patients with incarcerated and or strangulated hernia.

Costs

Conclusions

Level 1B: From the perspective of the hospital, an open mesh procedure is the most cost-effective operation in primary unilateral hernias. From a socio-economic perspective, an endoscopic procedure is probably the most cost-effective approach for patients who participate in the labour market, especially for bilateral hernias. In cost–utility analyses including quality of life (QALYs), endoscopic techniques (TEP) may be preferable, since they cause less numbness and chronic pain.

Recommendations

Grade A: It is recommended that, from a hospital perspective, an open mesh procedure is used for the treatment of inguinal hernia.
: From a socio-economic perspective, an endoscopic procedure is proposed for the active working population, especially for bilateral hernias.

Original article: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2719730/?tool=pmcentrez

Tags: meta analyses, Society, ehs school, Draft, Simons, inguinal

Laboratory Values for Clinical Investigations

Dr. Moro — Thu, 23 Jun 2011 12:31:17 +0000

These values summarize most of the laboratory values needed for investigations

Haematological values


	Reference range

Analysis	SI units	Non-SI units

Bleeding time (Ivy)	< 8 mins	-

Blood volume

Male	75 ± 10 mL/kg	-

Female	70 ± 10 mL/kg	-

Coagulation screen

Prothrombin time	10.5-13.5 secs	-

Activated partial thromboplastin time	26-36 secs	-

D-dimers

To detect disseminated intravascular coagulation	< 200 μg/L	< 200 ng/mL

To detect venous thromboembolism	< 500 μg/L	< 500 ng/mL

Erythrocyte sedimentation rate	Higher values in older patients are not necessarily abnormal

Adult male	0-10 mm/hr	-

Adult female	3-15 mm/hr	-

Ferritin

Male	20-300 μg/L	20-300 ng/mL

Female	14-150 μg/L	14-150 ng/mL

Fibrinogen	1.5-4.0 g/L	0.15-0.4 g/dL

Folate

Serum	5.0-20 μg/L	5.0-20 ng/mL

Red cell	257-800 μg/L	257-800 ng/mL

Haemoglobin

Male	130-180 g/L	13-18 g/dL

Female	115-165 g/L	11.5-16.5 g/dL

Haptoglobin	0.4-2.4 g/L	0.04-0.24 g/dL

Iron	10-32 μmol/L	56-178 μg/dL

Leucocytes (adults)	4.0-11.0 × 10⁹/L	4.0-11.0 × 10³/mm³

Differential white cell count

Neutrophil granulocytes	2.0-7.5 × 10⁹/L	2.0-7.5 × 10³/mm³

Lymphocytes	1.5-4.0 × 10⁹/L	1.5-4.0 × 10³/mm³

Monocytes	0.2-0.8 × 10⁹/L	0.2-0.8 × 10³/mm³

Eosinophil granulocytes	0.04-0.4 × 10⁹/L	0.04-0.4 × 10³/mm³

Basophil granulocytes	0.01-0.1 × 10⁹/L	0.01-0.1 × 10³/mm³

Mean cell haemoglobin (MCH)	27-32 pg	-

Mean cell volume (MCV)	78-98 fl	-

Packed cell volume (PCV) or haematocrit

Male	0.40-0.54	-

Female	0.37-0.47	-

Platelets	150-350 × 10⁹/L	150-350 × 10³/mm³

Red cell count

Male	4.5-6.5 × 10¹²/L	4.5-6.5 × 10⁶/mm³

Female	3.8-5.8 × 10¹²/L	3.8-5.8 × 10⁶/mm³

Red cell lifespan

Mean	120 days	-

Half-life (⁵¹Cr)	25-35 days	-

Reticulocytes (adults)	25-85 × 10⁹/L	25-85 × 10³/mm³

Transferrin	2.0-4.0 g/L	0.2-0.4 g/dL

Transferrin saturation

Male	25-56%	-

Female	14-51%	-

Vitamin B₁₂	251-900 ng/L	-

Cerebrospinal fluid analysis


	Reference range

Analysis	SI units	Non-SI units

Cells	< 5 × 10⁶ cells/L (all mononuclear)	< 5 cells/mm³

Glucose¹	2.3-4.5 mmol/L	41-81 mg/dL

IgG index²	< 0.65	-

Total protein	140-450 mg/L	0.014-0.045 g/dL

¹Interpret in relation to plasma glucose. Values in CSF typically approximately two-thirds plasma levels.
²A crude index of increase in IgG attributable to intrathecal synthesis.

Common analytes in urine


	Reference range

Analyte	SI units	Non-SI units

Albumin	Proteinuria is defined below

Calcium (normal diet)	Up to 7.5 mmol/24 hrs	Up to 15 meq/24 hrs or 3-300 mg/24 hrs

Copper	< 0.6 μmol/24 hrs	< 38 μg/24 hrs

Cortisol

Overnight (early morning sample)	< 20 nmol cortisol/mmol creatinine	< 67 μg cortisol/g creatinine

24-hr collection	25-250 nmol/24 hrs	9.1-91 μg/24 hrs

Creatinine	10-20 mmol/24 hrs	1130-2260 mg/24 hrs

5-hydroxyindole-3-acetic acid (5-HIAA)	10-42 μmol/24 hrs	1.9-8.1 mg/24 hrs

Metadrenalines

Normetadrenaline	0.4-3.4 μmol/24 hrs	73-620 μg/24 hrs

Metadrenaline	0.3-1.7 μmol/24 hrs	59-335 μg/24 hrs

Oxalate	0.04-0.49 mmol/24 hrs	3.6-44 mg/24 hrs

Phosphate	15-50 mmol/24 hrs	465-1548 mg/24 hrs

Potassium*	25-100 mmol/24 hrs	25-100 meq/24 hrs

Protein	< 0.3 g/L	< 0.03 g/dL

Sodium*	100-200 mmol/24 hrs	100-200 meq/24 hrs

Urate	1.2-3.0 mmol/24 hrs	202-504 mg/24 hrs

Urea	170-600 mmol/24 hrs	10.2-36.0 g/24 hrs

Other common analytes in venous blood in adults


	Reference range

Analyte	SI units	Non-SI units

α₁-antitrypsin	1.1-2.1 g/L	110-210 mg/dL

Alanine aminotransferase (ALT)	10-50 U/L	-

Albumin	35-50 g/L	3.5-5.0 g/dL

Alkaline phosphatase	40-125 U/L	-

Amylase	< 100 U/L	-

Aspartate aminotransferase (AST)	10-45 U/L	-

Bilirubin (total)	3-16 μmol/L	0.18-0.94 mg/dL

Calcium (total)	2.1-2.6 mmol/L	4.2-5.2 meq/L or 8.50-10.50 mg/dL

Carboxy-haemoglobin	0.1-3.0%	-

Caeruloplasmin	0.2-0.6 g/L	20-60 mg/dL

Cholesterol (total)	Ideal level varies according to cardiovascular risk so reference ranges can be misleading. The following values were described by the European Atherosclerosis Society:

	Mild increase

	5.2-6.5 mmol/L	200-250 mg/dL

	Moderate increase

	6.5-7.8 mmol/L	250-300 mg/dL

	Severe increase

	> 7.8 mmol/L	> 300 mg/dL

HDL-cholesterol	Ideal level varies according to cardiovascular risk so reference ranges can be misleading. According to the National Cholesterol Education Programme Adult Treatment Panel III (ATPIII), a low HDL-cholesterol is:

	< 1.0 mmol/L	< 40 mg/dL

Complement

C3	0.73-1.4 g/L	-

C4	0.12-0.3 g/L	-

Total haemolytic complement	0.086-0.410 g/L	-

Copper	13-24 μmol/L	83-153 μg/dL

C-reactive protein	< 5 mg/L Highly sensitive CRP assays also exist which measure lower values and may be useful in estimating cardiovascular risk

Creatine kinase (total)

Male	55-170 U/L	-

Female	30-135 U/L	-

Creatine kinase MB isoenzyme	< 6% of total CK	-

Ethanol	Not normally detectable

	Marked intoxication

	65-87 mmol/L	300-400 mg/dL

	Stupor

	87-109 mmol/L	400-500 mg/dL

	Coma

	> 109 mmol/L	> 500 mg/dL

Gamma-glutamyl transferase (GGT)	Male 10-55 U/L Female 5-35 U/L	-

Glucose (fasting)	3.6-5.8 mmol/L	65-104 mg/dL

Glycated haemoglobin (HbA_1c)	4.0-6.0% 20-42 mmol/mol Hb	-

Immunoglobulins (Ig)

IgA	0.8-4.5 g/L	-

IgE	0-250 kU/L	-

IgG	6.0-15.0 g/L	-

IgM	0.35-2.90 g/L	-

Lactate	0.6-2.4 mmol/L	5.40-21.6 mg/dL

Lactate dehydrogenase (total)	208-460 U/L	-

Lead	< 1.0 μmol/L	< 21 μg/dL

Magnesium	0.75-1.0 mmol/L	1.5-2.0 meq/L or 1.82-2.43 mg/dL

Osmolality	280-296 mmol/kg	-

Osmolarity	280-296 mosm/L	-

Phosphate (fasting)	0.8-1.4 mmol/L	2.48-4.34 mg/dL

Protein (total)	60-80 g/L	6-8 g/dL

Triglycerides (fasting)	0.6-1.7 mmol/L	53-150 mg/dL

Troponins	Values consistent with ‘myocyte necrosis’ or myocardial infarction are crucially dependent upon which troponin is measured (I or T) and on the method employed

Tryptase	0-135 mg/L	-

Urate

Male	0.12-0.42 mmol/L	2.0-7.0 mg/dL

Female	0.12-0.36 mmol/L	2.0-6.0 mg/dL

Vitamin D

25(OH)D	25-170 nmol/L	10-68 ng/mL

1,25(OH)₂D	20-120 pmol/L	7.7-46 pg/mL

Zinc	11-22 μmol/L	72-144 μg/dL

Hormones in venous blood


	Reference range

Hormone	SI units	Non-SI units

Adrenocorticotrophic hormone (ACTH) (plasma)	1.5-11.2 pmol/L (0700-1000 hrs)	7-51 pg/mL

Aldosterone

Supine	30-440 pmol/L	1.09-15.9 ng/dL

Erect	110-860 pmol/L	3.97-31.0 ng/dL

Cortisol	Dynamic tests are required

Follicle-stimulating hormone (FSH)

Male	1.0-10.0 U/L	0.2-2.2 ng/mL

Female	3.0-9.0 U/L (early follicular, luteal)	0.7-2.0 ng/mL

	< 30 U/L (mid-cycle)	< 6.7 ng/mL

	> 30 U/L (post-menopausal)	> 6.7 ng/mL

Gastrin (plasma, fasting)	< 57 pmol/L	< 120 pg/mL

Growth hormone (GH)	< 0.5 μg/L excludes acromegaly (if IGF1 in reference range)	-

	> 6 μg/L excludes GH deficiency

	Dynamic tests are usually required

Insulin	Highly variable and interpretable only in relation to plasma glucose and body habitus	-

Luteinising hormone (LH)

Male	1.0-9.0 U/L	0.11-1.0 μg/L

Female	2.5-9.0 U/L (early follicular, luteal)	0.3-1.0 μg/L

	Up to 90 U/L (mid-cycle)	Up to 10 μg/L

	> 20 U/L (post-menopausal)	> 2.2 μg/L

17β-Oestradiol

Male	< 160 pmol/L	< 43 pg/mL

Female	110-180 pmol/L (early follicular)	30-49 pg/mL

	550-2095 pmol/L (mid-cycle)	150-570 pg/mL

	370-770 pmol/L (luteal)	101-209 pg/mL

	< 150 pmol/L (post-menopausal)	< 41 pg/mL

Parathyroid hormone (PTH)	1.0-6.5 pmol/L	10-65 pg/mL

Progesterone

Male	< 2.0 nmol/L	< 0.63 ng/mL

Female	< 2.0 nmol/L (follicular)	< 0.63 ng/mL

	> 15 nmol/L (mid-luteal)	> 4.7 ng/mL

	< 2.0 nmol/L (post-menopausal)	< 0.63 ng/mL

Prolactin (PRL)	60-500 mU/L	-

Renin activity

Erect	1.0-4.2 ng/mL/hr	-

Supine	0.5-2.6 ng/mL/hr	-

Testosterone

Male	10-30 nmol/L	2.88-8.64 ng/mL

Female	0.4-3.0 nmol/L	0.12-0.87 ng/mL

Thyroid-stimulating hormone (TSH)	0.2-4.5 mU/L	-

Thyroxine (free) (free T₄)	9-21 pmol/L	700-1632 pg/dL

Triiodothyronine (T₃)	0.9-2.4 nmol/L	59-156 ng/dL

Notes

A number of hormones are unstable and collection details are critical to obtaining a meaningful result. Refer to local laboratory handbook.
Values in the table are only a guideline; hormone levels can often only be meaningfully understood in relation to factors such as sex (e.g. testosterone), age (e.g. FSH in women), time of day (e.g. cortisol) or regulatory factors (e.g. insulin and glucose, PTH and [Ca²⁺]).
Reference ranges may be critically method-dependent.

Urea and electrolytes in venous blood


	Reference range

Analysis	SI units	Non-SI units

Sodium	135-145 mmol/L	135-145 meq/L

Potassium (plasma)	3.3-4.7 mmol/L	3.3-4.7 meq/L

Potassium (serum)	3.6-5.1 mmol/L	3.6-5.1 meq/L

Chloride	95-107 mmol/L	95-107 meq/L

Urea	2.5-6.6 mmol/L	15-40 mg/dL

Creatinine	60-120 μmol/L	0.68-1.36 mg/dL

Arterial blood analysis


	Reference range

Analysis	SI units	Non-SI units

Bicarbonate	21-29 mmol/L	21-29 meq/L

Hydrogen ion	37-45 nmol/L	pH 7.35-7.43

Pa CO₂	4.5-6.0 kPa	34-45 mmHg

Pa O₂	12-15 kPa	90-113 mmHg

Oxygen saturation	> 97%

Tags: Copper, white cell count, pmol, clinical investigations, Creatine

Iron Deficiency Anaemia

Dr. Moro — Mon, 20 Jun 2011 17:07:51 +0000

This occurs when iron losses or physiological requirements exceed absorption.

Blood loss

The most common explanation in men and post-menopausal women is gastrointestinal blood loss. This may result from occult gastric or colorectal malignancy, gastritis, peptic ulceration, inflammatory bowel disease, diverticulitis, polyps and angiodysplastic lesions. On a world-wide basis, hookworm and schistosomiasis are the most prevalent causes of gut blood loss. Gastrointestinal blood loss may be exacerbated by the chronic use of aspirin or NSAIDs, which cause intestinal erosions and impair platelet function. In women of child-bearing age, menstrual blood loss, pregnancy and breastfeeding contribute to iron deficiency by depleting iron stores; in developed countries one-third of women in this age bracket have low iron stores but only 3% display iron-deficient haematopoiesis. Rarely, chronic haemoptysis or haematuria may cause iron deficiency.

Malabsorption

A dietary assessment should be made in all patients to ascertain their iron intake. Gastric acid is required to release iron from food and helps to keep iron in the soluble ferrous state. Hypochlorhydria in the elderly or that due to drugs such as proton pump inhibitors may contribute to the lack of iron availability from the diet, as may previous gastric surgery. Iron is absorbed actively in the upper small intestine and hence can be affected by coeliac disease. Anyone with features of malabsorption or recurrent deficiency in the absence of other explanations, young men with normal diet or young women with normal menstruation and diet in association with iron deficiency, should be screened for coeliac disease.

Iron absorption, uptake and distribution in the body.

Physiological demands

At times of rapid growth such as infancy and puberty, iron demands increase and may outstrip absorption. This may be exacerbated by prematurity and breastfeeding in infants or menstruation in girls. In pregnancy, iron is diverted to the fetus, the placenta and the increased maternal red cell mass, and is lost with bleeding at parturition. There is no consensus about the routine use of iron supplementation in pregnancy but if women with a poor dietary history or previous heavy menstrual losses become pregnant and the side-effects are acceptable, it is a justifiable practice.

Investigations

Confirmation of iron deficiency

Plasma ferritin is a measure of iron stores and the best single test to confirm iron deficiency. It is a very specific test; a subnormal level is due to iron deficiency, hypothyroidism or vitamin C deficiency. Levels can be raised by liver disease and in an acute phase response; in these conditions a ferritin level of up to 100 μg/l may still be associated with absent bone marrow iron stores. Plasma iron and total iron binding capacity (TIBC) are measures of iron availability, hence are affected by many factors besides iron stores. Plasma iron has a marked diurnal and day-to-day variation and becomes very low during an acute phase response but is raised in liver disease and haemolysis. Transferrin levels are lowered by malnutrition, liver disease, an acute phase response and nephrotic syndrome but raised by pregnancy or the oral contraceptive pill. A transferrin saturation of less than 16% is consistent with iron deficiency but is less specific than a ferritin measurement.

All proliferating cells express membrane transferrin receptors to acquire iron; a small amount of this receptor is shed into blood and found in a free soluble form there. At times of poor iron stores, cells up-regulate transferrin receptor expression; hence the levels of soluble plasma transferrin receptor increase. This can now be measured by immunoassay and used to distinguish storage iron depletion in the presence of an acute phase response or liver disease where a raised level indicates iron deficiency. In difficult cases it may still be necessary to examine a bone marrow aspirate for iron stores.

Investigation of the cause

This will depend upon the age and sex of the patient as well as the history and clinical findings. In men over the age of 40 years and in post-menopausal women with a normal diet, the upper and lower gastrointestinal tract should be investigated by endoscopy or barium studies. If coeliac disease is suspected, serum antigliadin and anti-endomysium antibodies and duodenal biopsy are indicated. In the tropics stool and urine should be examined for parasites.

Management

Unless the patient has angina, heart failure or evidence of cerebral hypoxia, transfusion is not necessary and oral iron supplementation is appropriate. Ferrous sulphate 200 mg 8-hourly (120 mg of elemental iron per day) is more than adequate and should be continued for 3-6 months to replete iron stores. The occasional patient is intolerant of ferrous sulphate, with dyspepsia and altered bowel habit. In this case a reduction in dose to 200 mg 12-hourly or a switch to ferrous gluconate 300 mg 12-hourly (70 mg of elemental iron per day) should be made. Delayed-release preparations are not useful since they release iron beyond the upper small intestine where it cannot be absorbed.

The haemoglobin should rise by 10 g/l every 7-10 days and a reticulocyte response will be evident by 1 week. A failure to respond adequately may be due to non-compliance, continued blood loss, malabsorption or an incorrect diagnosis. The occasional patient with malabsorption or chronic gut disease may need parenteral iron with deep intramuscular injection of iron sorbitol (1.5 mg of iron per kg body weight). This will produce a haematological response and rapidly replete iron stores. Patients should be warned that a brown skin discoloration like a tattoo is likely to develop at the sites of administration.

Tags: haematopoiesis, iron availability, loss

Parkinson’s Disease

Dr. Moro — Sun, 19 Jun 2011 19:27:45 +0000

Parkinson’s disease is a neurodegenerative condition which affects the basal ganglia and which presents with differing combinations of slowness of movement (bradykinesia), increased tone (rigidity), tremor and loss of postural reflexes. Parkinson’s disease has an annual incidence of about 0.2/1000 and a prevalence of 1.5/1000 in the UK. Prevalence rates are similar throughout the world, though lower rates have been reported for China and West Africa. Whilst 10% of the patients are under 45 years at presentation, the incidence and prevalence both increase with age, the latter rising to over 1% in those over 60. Sex incidence is about equal. It is less common in cigarette smokers. The outlook for patients with Parkinson’s disease is variable, and is related to age at onset. If symptoms start in middle life, the disease is usually steadily progressive and likely to shorten lifespan because of the complications of immobility and tendency to fall. Onset after 70 is unlikely to shorten life or become severe.

Parkinson's disease. High power (× 400) of substantia nigra of a patient with Parkinson's disease to show classical Lewy body (haematoxylin and eosin).

Pathophysiology

A small number of cases are familial in nature and mutations in several genes have now been identified as an underlying cause. However, in the majority the cause is unknown, and no strong genetic factors have been identified. The discovery that methyl-phenyl-tetrahydropyridine (MPTP) caused severe parkinsonism in young drug users suggests that the idiopathic disease might be due to an environmental toxin; many candidate toxins have been studied, but there is no strong evidence in favour of any of them. There are several features, including depletion of the pigmented dopaminergic neurons in the substantia nigra, hyaline inclusions in nigral cells (Lewy bodies), atrophic changes in the substantia nigra and depletion of neurons in the locus coeruleus. Reduced dopaminergic output from the substantia nigra to the globus pallidus leads to reduced inhibitory effects on the subthalamic nucleus, neurons of which become more active than usual in inhibiting activation of the cortex. This in turn results in bradykinesia.

Clinical features

The classical syndrome of tremor, rigidity and bradykinesia may be absent initially, when non-specific symptoms of tiredness, aching limbs, mental slowness, depression and small handwriting (micrographia) may be noticed. The presentation is almost always unilateral, a resting tremor in an upper limb being a common presenting feature. The tremor may eventually affect the legs, mouth and tongue. It may remain the predominant symptom for some years. Bradykinesia may develop gradually. Most patients have difficulty with rapid fine movements, and this manifests itself as slowness of gait and difficulty with tasks such as fastening buttons, shaving or writing. Rigidity, or increased muscular tone, causes stiffness and a flexed posture. Postural righting reflexes are impaired early on in the disease, but falls tend not to occur until later. As the disease advances, speech becomes softer and indistinct. There are a number of abnormalities on neurological examination, and these are listed below.

Although the features are initially unilateral, gradual bilateral involvement is the rule. Muscle strength and reflexes remain normal, and plantar responses are flexor. There is a paucity of facial expression (hypomimia) and the blink reflex may be exaggerated and fail to habituate (glabellar tap sign). Eye movements are normal to standard clinical testing, provided allowance is made for the normal limitation of upward gaze with age. Sensation is normal and intellectual faculties are not affected initially. As the disease progresses, about one-third of patients develop cognitive impairment.

Physical abnormalities in Parkinson’s disease

General

Expressionless face
Greasy skin
Soft, rapid, indistinct speech
Flexed posture
Impaired postural reflexes

Gait

Slow to start walking
Shortened stride
Rapid, small stride length, tendency to shorten (festination(
Reduced arm swing
Impaired balance on turning

Tremor: Resting (4-6 Hz)

Coarse, complex movements, usually first in fingers/thumb
- Flexion/extension of fingers
- Abduction/adduction of thumb
- Supination/pronation of forearm
May affect arms, legs, feet, jaw, tongue
Intermittent, present at rest and when distracted
Diminished on action

Postural (8-10 Hz)

Less obvious, faster, finer amplitude
Present on action or posture, persists with movement

Rigidity

Cogwheel type, mostly upper limbs
Plastic (lead pipe) type, mostly legs

Bradykinesia

Slowness in initiating or repeating movements
Impaired fine movements, especially of fingers

The diagnosis is made clinically, as there is no diagnostic test for Parkinson’s disease. Sometimes it is necessary to investigate patients to exclude other causes of parkinsonism if there are any unusual features. Patients presenting before the age of 50 are usually tested for Wilson’s disease, and imaging (CT or MRI) of the head may be needed if there are any features suggestive of pyramidal, cerebellar or autonomic involvement, or the diagnosis is otherwise in doubt.

Management

Drug therapy

Levodopa combined with a peripheral-acting dopa-decarboxylase inhibitor provides the mainstay of treatment in Parkinson’s disease but should only be started to help overcome significant disability. Other agents include anticholinergic drugs, dopamine receptor agonists, selegiline, COMT inhibitors and amantadine.

Mechanisms of drug action in Parkinson's disease. (1) Decarboxylase inhibitors (carbidopa and benserazide) decrease side-effects by reducing peripheral conversion of levodopa to dopamine by aromatic amino acid decarboxylase (AAAD). (2) Active transport of levodopa into the brain may be inhibited by competition from dietary amino acids after a high-protein meal. (3) In the nigrostriatal neurons, levodopa is converted into dopamine. (4) Amantadine enhances the release of dopamine at the nerve terminal. (5) Dopamine agonists act directly on striatal receptors. (6) The monoamine oxidase type B (MAO-B) inhibitor selegiline increases the availability of neuronal dopamine by reducing its metabolism outside the neuron. (7) The catechol-O-methyl-transferase (COMT) inhibitor entacapone prolongs the availability of dopamine by inhibiting the metabolism of dopamine and levodopa outside the neuron.

Levodopa

Although the number of dopamine-releasing terminals in the striatum is diminished in Parkinson’s disease, remaining neurons can be driven to produce more dopamine by administering its precursor, levodopa. If levodopa is administered orally, more than 90% is decarboxylated to dopamine peripherally in the gastrointestinal tract and blood vessels, and only a small proportion reaches the brain. This peripheral conversion of levodopa is responsible for the high incidence of side-effects if it is used alone. The problem is largely overcome by giving a decarboxylase inhibitor that does not cross the blood-brain barrier along with the levodopa. Two peripheral decarboxylase inhibitors, carbidopa and benserazide, are available as combination preparations with levodopa (as Sinemet and Madopar, respectively).

The initiation of levodopa therapy should be delayed until there is significant disability, since there is concern that its use makes long-term side-effects more likely. With this in mind, some authorities suggest that it is advisable to initiate treatment with a dopamine agonist (see below) or a slow-release preparation of levodopa in order to minimise or delay the onset of long-term side-effects, but evidence for this is not strong. The important point is to treat with as little medication as possible consistent with the patient being able to perform the activities of daily living. Levodopa is particularly effective at improving bradykinesia and rigidity. Tremor is also helped but rather unpredictably. The initial dose is 50 mg 8- or 12-hourly, increased if necessary. The total levodopa dose may be increased to over 1000 mg/day if necessary. Side-effects include postural hypotension, nausea and vomiting, which may be offset by the use of a peripheral dopamine antagonist such as domperidone. Other dose-related side-effects are involuntary movements, particularly orofacial dyskinesias, limb and axial dystonias, and occasionally depression, hallucinations and delusions. Unusual but important side-effects include change in personality with increased (sometimes pathological) gambling, hypersexuality and drug (levodopa)-seeking behaviour.

Late deterioration despite levodopa therapy occurs after 3-5 years in one-third to one-half of patients. Usually this manifests as fluctuation in response. The simplest form of this is end-of-dose deterioration due to progression of the disease and loss of capacity to store dopamine. More complex fluctuations present as sudden, unpredictable changes in response, in which periods of severe parkinsonism alternate with dyskinesia and agitation (the ‘on-off’ phenomenon). End-of-dose deterioration can often be improved by dividing the levodopa into smaller but more frequent doses, or by converting to a slow-release preparation. The ‘on-off’ phenomenon is difficult to treat, but sometimes subcutaneous injections of apomorphine (a dopamine agonist) are helpful to ‘rescue’ the patient rapidly from an ‘off’ period.

Involuntary movements (dyskinesia) may occur as a peak-dose phenomenon, or as a biphasic phenomenon (occurring during both the build-up and wearing-off phases). Management is difficult, but involves modifying the way levodopa is administered to obtain constant levels in the brain, and the use of alternative drugs, including amantadine and dopamine agonists. Continuous infusion of apomorphine may be particularly helpful in this situation.

Anticholinergic agents

These have a useful effect on tremor and rigidity, but do not help bradykinesia. They can be prescribed early in the disease before bradykinesia is a problem, but should be avoided in elderly patients in whom they cause confusion and hallucinations. Other side-effects include dry mouth, blurred vision, difficulty with micturition and constipation. Many anticholinergics are available-for example, trihexyphenidyl (benzhexol; 1-4 mg 8-hourly) and orphenadrine (50-100 mg 8-hourly).

Dopamine receptor agonists

Several of these drugs are now available. They all have slightly different activity at the various dopamine receptors in the brain. Apomorphine given alone causes marked vomiting and has to be administered parenterally. The vomiting can be overcome by the concomitant use of domperidone, and parenteral administration achieved through continuous subcutaneous infusion from a portable pump, or by direct injection as needed. This requires considerable nursing support but, used correctly, can be very useful.

More easily administered drugs include bromocriptine, lisuride, pergolide, cabergoline, ropinirole and pramipexole, which can all be taken orally, and rotigotine which can be administered as a transdermal patch. These drugs are less powerful than levodopa in controlling features of parkinsonism, but they are much less likely to cause dose fluctuations or dyskinesia, though they will certainly exacerbate the latter once these have developed. Side-effects include nausea, vomiting, confusion and hallucinations. The dose of bromocriptine is 1 mg initially, increased to 2.5 mg 8-hourly, and thereafter up to 30 mg/day. Pergolide dose starts at 50 μg, increased to 250 μg 8-hourly, and possibly to 3000 μg/day. Dopamine agonists derived from ergot (pergolide and cabergoline) have recently been associated with the development of fibrotic reactions and thickening of heart valves. For this reason, the use of these agents is not advised.

Amantadine

This has a mild, usually short-lived effect on bradykinesia, but may be used early in the disease before more potent treatment is needed. Amantadine can be particularly useful in controlling the dyskinesias produced by dopaminergic treatment later in the disease. The dose is 100 mg 8- or 12-hourly. Side-effects include livedo reticularis, peripheral oedema, confusion and seizures.

Selegiline

Selegiline has a mild therapeutic effect in its own right. An early suggestion that it slows the progression of the disease has been discredited, as has the suggestion that it might be associated with an increased risk of sudden death. The usual dose is 5-10 mg in the morning.

COMT (catechol-O-methyl-transferase) inhibitors

Entacapone (200 mg with each dose of levodopa) prolongs the effects of each dose and reduces motor fluctuations when used with levodopa. This allows the levodopa dose to be reduced and given less frequently.

Surgery

Stereotactic thalamotomy can be used to treat tremor, though this is needed relatively infrequently because of the medical treatments available. Other stereotactic lesions are currently undergoing evaluation, in particular the implantation of stimulating electrodes into the globus pallidus to help in the management of drug-induced dyskinesia. The implantation of fetal mid-brain cells into the basal ganglia to enhance dopaminergic activity remains experimental.

Physiotherapy and speech therapy

Patients at all stages of Parkinson’s disease benefit from physiotherapy, which helps reduce rigidity and corrects abnormal posture. Speech therapy may help in patients where dysarthria and dysphonia interfere with communication.

Recent Approaches for Parkinson’s Disease Therapy

Physical abnormalities in Parkinson’s disease

General

· Expressionless face

· Greasy skin

· Soft, rapid, indistinct speech

· Flexed posture

· Impaired postural reflexes

Gait

· Slow to start walking

· Shortened stride

· Rapid, small stride length, tendency to shorten (festination(

· Reduced arm swing

· Impaired balance on turning

Tremor: Resting (4-6 Hz)

· Coarse, complex movements, usually first in fingers/thumb

o Flexion/extension of fingers

o Abduction/adduction of thumb

o Supination/pronation of forearm

· May affect arms, legs, feet, jaw, tongue

· Intermittent, present at rest and when distracted

· Diminished on action

Postural (8-10 Hz)

· Less obvious, faster, finer amplitude

· Present on action or posture, persists with movement

Rigidity

· Cogwheel type, mostly upper limbs

· Plastic (lead pipe) type, mostly legs

Bradykinesia

· Slowness in initiating or repeating movements

· Impaired fine movements, especially of fingers

Tags: COMT, postural reflexes, conversion, basal ganglia

Rheumatic Fever

Dr. Moro — Sun, 19 Jun 2011 14:19:04 +0000

Rheumatic fever (RF) is an acute inflammatory disease of children and young adults caused by infection with pharyngeal strains of Group A beta-haemolytic streptococci (serotypes 3, 5, 18, 24). It is due to an autoimmune reaction triggered by molecular mimicry between the M proteins of the infecting streptococci and cardiac myosin and the sarcolemmal membrane protein, laminin. During active carditis, helper CD4 lymphocytes increase in number, and the ratio of CD4 to CD8 cells increases in the heart valves and peripheral blood. All patients with acute RF demonstrate a non-HLA alloantigen which is expressed on the B cells (D8/17). HLA-DR1, 2, 3, 4, 7 and 53 have also been linked to the occurrence of acute RF. The time taken for rheumatic fever (RF) to develop after an attack of streptococcal pharyngitis is about 2 weeks. The disease is common in situations where there is overcrowding and poor sanitation. RF mainly affects the joints and heart. It is the large joints that are affected, as opposed to rheumatoid arthritis where small joints are predominantly involved. Other organs affected are the central nervous system and skin. Valvular heart disease, which is chronic and progressive, is the end result in about 50% of those affected. There is no gender predilection, but mitral stenosis and chorea occur more commonly in females. About 1.5 million people develop rheumatic heart disease in India. It also occurs with increasing frequency among native peoples of Australia and New Zealand.

The characteristic lesion of RF is the Aschoff nodule, which is a granulomatous lesion. It is composed of an area of central fibrinoid necrosis surrounded by multinucleated giant cells which have elongated nuclei with a distinct chromatin pattern, macrophages and T lymphocytes.

The diagnosis of acute rheumatic fever is based on revised Duckett Jones criteria plus evidence of preceding streptococcal infection. This includes a history of recent scarlet fever, an anti-streptolysin O titre (ASO titre) >250 Todd units in adults and >333 in children or a positive rapid streptococcal antigen test or throat culture. Other tests are anti-hyaluronidase, anti-DNase, anti-streptokinase and the Streptozyme test.

Clinical features

The clinical features of carditis include chest pain, pericardial rub and effusion, tachycardia out of proportion to fever, muffled heart sounds, a gallop rhythm, low cardiac output and, rarely, syncope. Cardiomegaly may occur.

Endocarditis is characterized by fever and changing murmurs.

The pansystolic murmur of mitral regurgitation is the most common while a mid-diastolic murmur at the apex (Carey Coombs murmur) due to acute rheumatic valvulitis and an early diastolic murmur of aortic regurgitation may also occur.

Congestive heart failure with hepatic congestion is a recognized feature. Cardiac failure is often due to valve dilatation and not myocarditis. ST and T wave changes, reduction in QRS voltages, first-degree atrioventricular block and other conduction defects may be seen in the electrocardiogram.

Subcutaneous nodules usually occur over bony prominences such as the olecranon, external occipital protuberance and vertebral bodies. They measure 0.5-2 cm in size, and are firm and painless. Their presence is strongly associated with carditis. Nodules may also occur over joints and tendons, and have a histological appearance resembling Aschoff nodules.

Arthritis seen in rheumatic fever is classically a polyarthritis that is migratory in nature. Large joints are predominantly affected, especially knees (75%) and ankles (50%). Deformities are not a feature of rheumatic arthritis, except in rare cases of the so-called ‘Jaccoud’s arthritis’ where periarticular fibrosis causes deformity of the metacarpo-phalangeal joints.

Erythema marginatum is very uncommon in South Asia although it is present in 10-20% of patients in the West. It is a transient, evanescent, non-itchy rash with elevated edges and a fading centre. The rash extends centrifugally to become circinate or leaf-like. The trunk is commonly affected and the face is characteristically spared.

Chorea (Sydenham’s or St. Vitus’ dance) is a late manifestation of rheumatic fever and occurs 3-6 months after its onset. The movements are described as rapid, jerky, irregular, non-repetitive, involuntary and semi-purposive, and disappear during sleep. Other features include emotional lability, hypotonia, pendular knee jerks, a ‘Jack in the box’ or darting tongue, speech disturbances and ‘milkmaid’s’ grip. Rheumatic chorea does not usually affect adult males. About 25% of patients with chorea eventually develop chronic valvular heart disease.

Pneumonia, pleural effusions, abdominal pain (due to mesenteric adenitis) and recurrent epistaxis have also been reported in association with rheumatic fever.

Treatment

Acute rheumatic fever is treated with bed rest and procaine penicillin 0.6 mega units intramuscularly daily or phenoxymethyl penicillin 500 mg orally four times daily, for 8 days.

A single dose of benzathine penicillin 1.2 mega units intramuscularly has also been advocated. Patients allergic to penicillin can be given erythromycin or tetracycline 500 mg four times daily for the same period.

Patients with arthritis should be treated with high dose salicylates (aspirin 100 mg/kg bodyweight/day up to 6-8 g/day, tapering the dose after 2 weeks to 60 mg/kg bodyweight/day for 6 weeks). Aspirin is sometimes given to the limit of tolerance determined by the development of tinnitus. The arthritis of rheumatic fever responds dramatically to salicylates, and failure to respond should make one suspect the accuracy of the diagnosis (‘salicylate test’).

Steroids in the form of prednisolone 1-2 mg/kg bodyweight/day are given when carditis is present, and slowly tapered off over 2-4 weeks. Steroids may be overlapped with aspirin during the tapering period. Intravenous steroids can be used in fulminant carditis.

Chorea is treated by nursing the patient in a quiet environment and with drugs such as haloperidol or other sedatives when required. Carbamazepine and valproic acid have been found to be very effective in the treatment of chorea.

Prophylaxis

All patients with rheumatic fever should be given long-term penicillin prophylaxis for prevention of recurrence of rheumatic fever. Prophylaxis is given in the form of benzathine penicillin 1.2 mega units by deep intramuscular injection into the gluteal region, once every 3 weeks. As an alternative, phenoxymethyl penicillin may be given at a dose of 250 mg orally twice a day. Patients allergic to penicillin should be given sulfadiazine 0.5-1 g orally once daily depending on their bodyweight. Erythromycin is reserved for patients who are allergic to both penicillin and sulfonamides. Prophylaxis is life-long if rheumatic carditis has occurred and in the presence of chronic rheumatic heart disease. In other cases, prophylaxis should be given until the patient reaches the age of 40 years or for 5 years after the last attack of rheumatic fever, whichever is the longer period. Prophylaxis for rheumatic fever does not exempt patients with chronic rheumatic valvular heart disease from requiring prophylaxis for infective endocarditis.

Prognosis

Fifty per cent of patients with acute rheumatic fever will eventually develop chronic rheumatic valvular heart disease after 10-20 years. This most commonly affects the mitral valve, followed by the aortic valve. The tricuspid valve is rarely affected, and the pulmonary valve is hardly ever affected. In the Indian subcontinent the development of valvular heart disease occurs at a much younger age. It may at times occur in children less than 10 years of age (juvenile mitral stenosis). However, only about 50% of persons with established rheumatic heart disease give a history of acute rheumatic fever. This may be due to the trivial or mild nature of rheumatic fever in some individuals.

Tags: group, disease, poor sanitation, lesion, mitral stenosis, reaction

Disease-modifying anti-rheumatic drugs (DMARDs)

Dr. Moro — Sun, 19 Jun 2011 11:18:21 +0000

Drug	Dose	Side-effects	Monitoring to detect side-effects
Sulfasalazine (enteric coated)	500 mg daily after food, increasing to 2-3 g daily	Nausea Skin rashes and mouth ulcers
		Neutropenia and/or thrombocytopenia	Initial, 2 weeks, then 4-monthly
		Abnormal liver biochemistry	Initial, 2 weeks, then 4-monthly
Methotrexate	2.5 mg increasing to 25 mg weekly, orally or s.c.	Nausea, mouth ulcers and diarrhoea
		Abnormal liver biochemistry	Initial, 2 weeks, then monthly
		Neutropenia and/or thrombocytopenia	Initial, weekly, then monthly
		Renal impairment	Initial, then every 3-6 months
		Pulmonary fibrosis (rare)	Baseline chest X-ray
Leflunomide	100 mg daily for 1-3 days, then 20 (or 10) mg daily or 10-20 mg daily	Diarrhoea
		Neutropenia and/or thrombocytopenia	Initial, then 2 weekly; monthly at 6 months
		Abnormal liver biochemistry	Initial, then 2 weekly; monthly at 6 months
		Alopecia
		Hypertension
TNF-α blockers		For all
Etanercept (alone or with methotrexate)	s.c. 25 mg × 2 weekly or 50 mg weekly	Injection site reactions Infections, e.g. TB and septicaemia	See British Society for Rheumatology Guidelines
Adalimumab (with methotrexate)	s.c. 40 mg alternate weeks	Hypersensitivity reactions Heart failure	www.rheumatology.org.uk/ guidelines/clinicalguidelines
		Rare – demyelination and autoimmune syndromes	Stop if no response after6 months
Infliximab (with methotrexate)	i.v. 3-10 mg/kg every 4-8 weeks	Reversible lupus-like syndrome
Other biological agents (used with methotrexate)
Anakinra	1 mg/kg s.c. daily	Injection site reaction Serious reactions – rare	Used after failure of anti-TNF agents
Rituximab	i.v. 500-1000 mg	Hypo/hypertension, skin rash, nausea, pruritis, back pain Rare – toxic epidermal necrolysis
Abatacept	i.v. 10 mg/kg on days 1, 15, 30 and then monthly	Nausea, vomiting Headache Hypersensitivity – rare
Tocilizumab	i.v. 8 mg/kg infusion	Headache, skin eruption, stomatitis, fever, anaphylactic reactions	Phase III studies

Tags: abatacept, chest, Hypersensitivity, injection, Sulfasalazine, impairment

Immune (Idiopathic) thrombocytopenia (ITP)

Dr. Moro — Sat, 18 Jun 2011 19:02:36 +0000

Immune thrombocytopenia (also called idiopathic thrombocytopenic purpura) is the commonest cause of thrombocytopenia in childhood. It has an incidence of around 4 per 100000 children per year. It is caused by immune-mediated destruction of circulating platelets due to anti-platelet autoantibodies. The reduced platelet count is accompanied by a compensatory increase of megakaryocytes in the bone marrow.

Clinical features

Causes of purpura or easy bruising

Platelet count reduced, i.e. thrombocytopenia
Increased platelet destruction or consumption
Immune	ITP (immune thrombocytopenia)
	SLE (systemic lupus erythematosus)
	Alloimmune neonatal thrombocytopenia
Non-immune	Haemolytic uraemic syndrome
	Thrombotic thrombocytopenic purpura
	DIC (disseminated intravascular coagulation)
	Congenital heart disease
	Giant haemangiomas (Kasabach-Merritt syndrome)
	Hypersplenism
Impaired platelet production
Congenital	Fanconi anaemia
	Wiskott-Aldrich syndrome
	Bernard-Soulier syndrome
Acquired	Aplastic anaemia
	Marrow infiltration (e.g. leukaemia)
	Drug-induced
Platelet count normal
Platelet dysfunction
Congenital	Rare disorders, e.g. Glanzmann’s thromboasthenia
Acquired	Uraemia, cardiopulmonary bypass
Vascular disorders
Congenital	Rare disorders, e.g. Ehlers-Danlos, Marfan’s syndrome, hereditaryhaemorrhagic telangiectasia
Acquired	Meningococcal and other severe infections Vasculitis, e.g. Henoch-Schönlein purpura, SLE Scurvy

Most children present between the ages of 2 and 10 years, with onset often 1-2 weeks after a viral infection. There is usually a short history of days or weeks. Affected children develop petechiae and purpura and superficial bruising (see Case history). It can cause epistaxis and other mucosal bleeding but profuse bleeding is uncommon despite the fact that the platelet count often falls to < 10 × 10⁹/L. Intracranial bleeding is a serious but rare complication, occurring in 0.1-0.5%, mainly in those with a long period of severe thrombocytopenia.

Diagnosis

ITP is a diagnosis of exclusion, so careful attention must be paid to the history, clinical features and blood film to ensure that another more sinister diagnosis is not missed. In the younger child a congenital cause (such as Wiskott-Aldrich or Bernard-Soulier syndromes) should be considered. Any atypical clinical features, such as the presence of hepatosplenomegaly or marked lymphadenopathy, should prompt a bone marrow examination to exclude acute leukaemia or aplastic anaemia. A bone marrow examination should also be performed if the child is going to be treated with steroids since this treatment may temporarily mask these diagnoses. SLE (systemic lupus erythematosus) should also be considered. However, if the clinical features are characteristic, with no abnormality in the blood other than a low platelet count and no intention to treat, there is no need to examine the bone marrow.

Management

Sian, aged 5 years, developed bruising and a skin rash over 24 hours. She had had an upper respiratory tract infection the previous week. On examination she appeared well but had a purpuric skin rash with some bruises on the trunk and legs (Fig. 22.19). There were three blood blisters on her tongue and buccal mucosa, but no fundal haemorrhages, lymphadenopathy or hepatosplenomegly. Urine was normal on stix testing. A full blood count showed Hb 11.5 g/dl with normal indices, WBC and differential normal, platelet count 17 × 10⁹/L. The platelets on the blood film were large; the film was otherwise normal. A diagnosis of ITP was made and she was discharged home. Her parents were counselled and given emergency contact names and telephone numbers. They were also given literature on the condition and advised that she should avoid contact sports but should continue to attend school. Over the next 2 weeks she continued to develop bruising and purpura but was asymptomatic. By the third week she had no new bruises, and her platelet count was 25 × 10⁹/L; the blood count and film showed no new abnormalities. The following week, the platelet count was 74 × 10⁹/L and a week later it was 200 × 10⁹/L. She was discharged from follow-up.

In immune thrombocytopenic purpura, in spite of impressive cutaneous manifestations and extremely low platelet count, the outlook is good and most will remit quickly without any intervention.

Bruising and purpura from immune thrombocytopenic purpura.

Case History

Immune thrombocytopenic purpura (ITP) treatment, and the child should avoid trauma, as far as possible, and contact sports while the platelet count is a very low.

In about 80% of children, the disease is acute, benign and self-limiting, usually remitting spontaneously within 6-8 weeks. Most children can be managed at home and do not require hospital admission. Treatment is controversial. Most children do not need any therapy even if their platelet count is <10 × 10⁹/L but treatment should be given if there is evidence of major bleeding (e.g. intracranial or gastrointestinal haemorrhage) or persistent minor bleeding (e.g. persistent oral bleeding). The treatment options are oral prednisolone or intravenous immunoglobulin, but both have significant side-effects and do not alter the chance of achieving complete remission. Immunoglobulin infusions usually result in a more rapid rise in the platelet count than steroids. Platelet transfusions are reserved for life-threatening haemorrhage as they raise the platelet count only for a few hours. The prednisolone should be given only as a short course, irrespective of the platelet count. The parents need immediate 24-hour access to hospital

Chronic ITP

In 20% of children the platelet count remains low 6 months after diagnosis; this is known as chronic ITP. No treatment is given unless there is major bleeding. As for acute ITP, long-term steroid treatment should not be used. Therefore treatment is mainly supportive, the child should avoid contact sports but be encouraged to continue normal activities, including schooling. As with acute ITP, parents need 24-hour access to hospital. The family may benefit from the parent ITP Support Group. Most children remit within 3 years from onset or stabilise with moderate, asymptomatic thrombocytopenia. Children with significant bleeding are rare and require specialist care. Splenectomy is probably the most effective treatment for this group, but has significant morbidity and may be unsuccessful in up to 25% of cases. If ITP in a child becomes chronic, regular screening for SLE should be performed, as the thrombocytopenia may predate the development of autoantibodies.

Tags: treatment, ehlers danlos, diagnosis

Recognizing Pneumothorax

Dr. Moro — Fri, 17 Jun 2011 16:53:14 +0000

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Tags: Draft, Recognizing, Auto, click, Pneumothorax, view

How To Recognize a Pleural Effusion

Dr. Moro — Fri, 17 Jun 2011 15:01:56 +0000

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Tags: view, Recognize, Draft, effusion, click, Pleural

Pulmonary Function Testing

Dr. Moro — Fri, 17 Jun 2011 13:34:44 +0000

In clinical practice, airflow limitation can be assessed by relatively simple tests that have good intra-subject repeatability. Normal values are required for their interpretation since these tests vary considerably, not only with sex, age and height, but also between individuals of the same age, sex and height. The standard deviation about the mean for a group of individuals is therefore very high; for example, the standard deviation for the peak expiratory flow rate is approximately 50 L/min, and for the FEV₁ it is approximately 0.4 L. Repeated measurements of lung function are useful for assessing the progression of disease in an individual patient.

Tests of ventilatory function

These tests are used mainly to assess the degree of airflow limitation present during expiration.

Test	Use	Advantages	Disadvantages
PEFR	Monitoring changes in airflow limitation in asthma	Portable Can be used at the bedside	Effort-dependent Poor measure of chronic airflow limitation
FEV, FVC, FEV₁/FVC	Assessment of airflow limitation The best single test	Reproducible Relatively effort-independent	Bulky equipment but smaller portable machines available
Flow-volume curves	Assessment of flow at lower lung volumes Detection of large airway obstruction both intra- and extrathoracic (e.g. tracheal stenosis, tumour)	Recognition of patterns of flow-volume curves for different diseases	Sophisticated equipment needed for full test but expiratory loop now possible with compact spirometry
Airways resistance	Assessment of airflow limitation	Sensitive	Technique difficult to perform
Lung volumes	Differentiation between restrictive and obstructive lung disease	Effort-independent, complements FEV₁	Sophisticated equipment needed
Gas transfer	Assessment and monitoring of extent of interstitial lung disease and emphysema	Non-invasive (compared with lung biopsy or radiation from repeated chest X-rays and CT)	Sophisticated equipment needed
Blood gases	Assessment of respiratory failure	Can detect early lung disease when measured during exercise	Invasive
Pulse oximetry	Postoperative, sleep studies and respiratory failure	Continuous monitoring Non-invasive	Measures saturation only
Exercise tests (6-min walk)	Practical assessment for disability and effects of therapy	No equipment required	Time-consuming Learning effect At least two walks required
Cardiorespiratory assessment	Early detection of lung/heart disease Fitness assessment	Differentiates breathlessness due to lung or heart disease	Expensive and complicated equipment required

Peak flow measurements. (a) Peak flow meter: the lips should be tight around the mouthpiece. (b) Graph of normal readings for men and women.

Peak expiratory flow rate (PEFR)

This is an extremely simple and cheap test. Subjects are asked to take a full inspiration to total lung capacity and then blow out forcefully into the peak flow meter, which is held horizontally. The lips must be placed tightly around the mouthpiece. The best of three tests is recorded.

Although reproducible, PEFR is not a good measure of airflow limitation since it measures the expiratory flow rate only in the first 2 ms of expiration and overestimates lung function in patients with moderate airflow limitation. PEFR is best used to monitor progression of disease and its treatment. Regular measurements of peak flow rates on waking, during the afternoon, and before bed demonstrate the wide diurnal variations in airflow limitation that characterize asthma and allow an objective assessment of treatment to be made.

Tags: FEV, obstructive lung disease, lung volumes, technique, flow, interstitial lung disease