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For Claire, Mum and Dad, your unwavering support makes endeavours like this possible. To my children, Joseph and Amelia – follow your dreams; anything is possible. GK
For all of our patients. May this book improve both your safety and your experience of anaesthesia. BJP
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and
Richard Wadsworth, Greg Cook, Andrew Roscoe, Zoka Milan, Ross Macnab and Kailash Bhatia
Cyprian Mendonca, Narcis Ungureanu, Aleksandra Nowicka, William Tosh, Benjamin Robinson and Carol L Bradbury
Baha Al-Shaikh, Sarah Hodge, Sanjay Agrawal, Michele Pennimpede, Sindy Lee, Janine MA Thomas and John Coombes
Baha Al-Shaikh, Sanjay Agrawal, Sindy Lee, Daniel Lake, Nessa Dooley, Simon Stacey, Maureen Bezzina and Gregory Waight
Preface
Welcome to the fourth edition of the Handbook of Clinical Anaesthesia. We have retained the overall structure as in the first three editions. The book continues to be a collection of individual entries each covering a particular topic, condition or problem which may be encountered in clinical anaesthesia. The philosophy of the book has been retained in that all of the information is presented in a concise form without unnecessary information or ‘padding’.
Over its lifespan between the first and the fourth editions, this book has undergone a significant evolution which we believe has served to improve it. The original idea was conceived by John Goldstone and Brian J Pollard in 1994. John unfortunately had to withdraw from the project at the second edition. For the fourth edition a second editor has been introduced again, Dr Gareth Kitchen. The choice of Gareth is clear. He is a young academic anaesthetist who has been able to instil new thoughts into the book and assist in driving it forwards and bringing on board a number of new names as experts in their fields.
In the first two editions, the authors of the various sections and monographs were drawn almost exclusively from the UK. In the third edition, the authorship was widened into a much more international field. In this fourth edition, we have returned to it being a UK-based field for the authors. Not only that but as we, the editors, are based in the Northwest, we
have selected our authors principally from this area as there is a huge amount of expertise here.
Remember that this book is not an exhaustive treatise. It does not cover every eventuality; no book can do that. The Handbook of Clinical Anaesthesia is a distillation of facts and guidance and is intended to complement the major texts in the subject. Individual entries are referenced where appropriate but the references are limited to a small number of key sources and include up-to-date reviews wherever possible.
Over the years this book has proved popular with trainees preparing for examinations in the speciality. It has also proved very popular with established consultants and specialists who keep it beside the phone, on the office desk or in the operating theatre suite for straightforward advice on problems or situations encountered.
Finally, we would like to pay tribute to the many authors involved in the first three editions of this book. A significant proportion of their text and information has been retained where the advice has not materially changed. Many sections have nevertheless been rewritten as appropriate and updated as necessary. The authors involved in the first three editions are too numerous to mention but to each and every one we thank you for your input to the previous editions and hope that you approve of this new version and its updated information.
BJP and GK
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Contributors
Sanjay Agrawal FRCA
Specialist Registrar
William Harvey Hospital Ashford, Kent, UK
Baha Al-Shaikh FRCA FCAI
Consultant Anaesthetist and Visiting Professor
William Harvey Hospital Ashford, Kent, UK
Kailash Bhatia MBBS FRCA EDRA DA DNB
Consultant Anaesthetist
Central Manchester University Hospitals and St Mary’s Hospital Manchester, UK
Maureen Bezzina MD
Specialist Registrar
William Harvey Hospital
Ashford, Kent, UK
Katherine Bexon BMedSci BMBS FRCA
Consultant in Anaesthesia
Central Manchester University Hospitals
NHS Foundation Trust Manchester, UK
Carol L Bradbury FRCA
Specialist Registrar in Anaesthesia University Hospitals Coventry and Warwickshire Coventry, UK
Eleanor Chapman MBChB BSc FRCA
Consultant Anaesthetist
Salford Royal Foundation Trust
Salford, UK
Sofia Clegg MbChB FRCA
Consultant in Anaesthesia
Central Manchester University Hospitals
NHS Foundation Trust Manchester, UK
Greg Cook MBChB FRCA FFICM
Consultant in Anaesthesia and Intensive Care
Medicine
Manchester Royal Infirmary Manchester, UK
John Coombes MBBS FCAI
Specialist Registrar
William Harvey Hospital Ashford, Kent, UK
Sophie Kimber Craig MBChB FRCA
Consultant Anaesthetist
Bolton NHS Foundation Trust Bolton, UK
Nessa Dooley FRCA
Clinical Fellow
Bart’s Heart Centre London, UK
Alastair Duncan MBChB MSc FRCA
Specialty Trainee in Anaesthesia North West Deanery, UK
Amy Hobbs MBChB BSc FRCA
Consultant Anaesthetist
Bolton NHS Foundation Trust Bolton, UK
Sarah Hodge FRCA
Specialist Registrar
William Harvey Hospital Ashford, Kent, UK
Adel Hutchinson MBChB BSc (hons) FRCA
Consultant in Anaesthesia
Central Manchester University Hospitals NHS Foundation Trust Manchester, UK
Contributors
Matthew James Jackson BSc (Hons) MBChB
FFICM FRCA
Consultant in Intensive Care Medicine and Anaesthesia
Stockport NHS Foundation Trust
Stockport, UK
Gareth Kitchen MBChB FRCA
Medical Research Council
Clinical Research Training Fellow
The University of Manchester and Anaesthesia Trainee
North Western Deanery
Honorary Registrar
Central Manchester Foundation Trust and University Hospital of South Manchester Manchester, UK
Daniel Lake MBBS iBSc FRCA
Specialist Registrar
William Harvey Hospital
Ashford, UK
Sindy Lee MBBS
CT2 Anaesthetics
Queen Elizabeth The Queen Mother Hospital
Margate, Kent, UK
Bernadette Lomas BSc(MedSci) MBChB FRCA
ALCM PGCert (Med ED)
Specialty Registrar
North West School of Anaesthesia
Honorary Lecturer
University Hospital of South Manchester Manchester, UK
John-Paul Lomas BSc(MedSci) MBChB FRCA
FFICM PGCertMedEd
Consultant in Anaesthesia and Intensive Care Medicine
Bolton NHS Foundation Trust Bolton, UK
Robert Peter Loveridge MBChB PgCert MedEd
FRCA
Locum Consultant Anaesthetist
Stockport NHS Foundation Trust
Stockport, UK
Ross Macnab BSc MBChB FRCA
Consultant in Anaesthesia
Manchester Royal Infirmary Manchester, UK
Cyprian Mendonca MD FRCA
Consultant Anaesthetist and Honorary Senior Clinical Lecturer
University Hospitals Coventry and Warwickshire and
Featherstone Professor, AAGBI, 2016-18
Honorary Associate Professor and Consultant
Anaesthetist
University Hospitals Coventry and Warwickshire
NHS Trust
Coventry, UK
Zoka Milan PhD FRCA FCIM
Visiting Professor
Consultant Anaesthetist and Intensivist, and Honorary Senior Lecturer
King’s College Hospital London, UK
Aleksandra Nowicka MD FRCA
Speciality Registrar in Anaesthesia
Warwickshire School of Anaesthesia
Warwick, UK
Santosh Patel MD FRCA
Consultant Anaesthetist
The Pennine Acute Hospitals NHS Trust
Rochdale, UK and
Honorary Senior Lecturer
Faculty of Medical and Human Sciences
University of Manchester
Michele Pennimpede MD
Anaesthetic Speciality Doctor
William Harvey Hospital
Ashford, Kent, UK
Brian J Pollard BPharm MBChB MD FRCA
Emeritus Professor of Medical Education
Formerly Professor of Anaesthesia
Consultant Anaesthetist and Intensivist
The University of Manchester Manchester, UK
Benjamin Robinson
Specialist Registrar in Anaesthesia Warwickshire School of Anaesthesia Warwick, UK
Andrew Roscoe MBChB FRCA
Consultant in Anaesthesia and Intensive Care Medicine
Papworth Hospital Cambridge, UK
Patrick Ross MB BCh BAO BA FRCA PGDipME
Honorary Senior Lecturer
Manchester Medical School and
Consultant Anaesthetist
Pennine Acute Hospitals NHS Trust Manchester, UK
Clifford Shelton MSc MBChB PGCertMedEd FHEA FRCA MAcadMedEd NIHR Doctoral Research Fellow Lancaster Medical School Lancaster, UK and
Anaesthetic Registrar
University Hospital South Manchester Wythenshawe, UK
Roger Martin Slater MBChB FRCA MRCP(UK) FFICM
Consultant Anaesthetist
Princess Royal Hospital Telford, UK
Simon Stacey FRCA
Consultant Anaesthetist
St Bartholomew’s Hospital London, UK
Matthew Stagg MBChB FRCA
Consultant in Cardiothoracic Anaesthesia and Intensive Care
Blackpool Victoria Hospital Blackpool, UK
Janine MA Thomas MBBS DM MBA
Speciality Doctor
William Harvey Hospital Ashford, Kent, UK
William Tosh MBChB FRCA
Specialist Registrar in Anaesthesia University Hospitals Coventry and Warwickshire Coventry, UK
Redmond P Tully MBBS BSc FFICM EDRA FRCA
Consultant in Anaesthesia and Intensive Care Medicine
Royal Oldham Hospital Oldham, UK
Robert Turner BMBCh Bsc
Specialist Anaesthetics Trainee
St Vincent’s University Hospital Dublin, Ireland
Narcis Ungureanu MD DESA EDRA FRCA
University Hospitals Coventry and Warwickshire Coventry, UK and
Burton Hospitals NHS Foundation Trust UK
Akbar Vohra MBChB DA FRCA FFICM
Honorary Senior Lecturer
University of Manchester Consultant in Cardiac Anaesthesia and Intensive Care
Manchester Royal Infirmary Manchester, UK
Richard Wadsworth BSc MB BChir FRCA Consultant in Anaesthesia
Manchester Royal Infirmary Manchester, UK
Gregory Waight FRCA Specialist Registrar
William Harvey Hospital Ashford, Kent, UK
Tom Wright
Speciality Trainee in Anaesthesia
Northwest Deanery Specialty, UK
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List of abbreviations
A&E Accident & Emergency
AAGBI Association of Anaesthetists of Great Britain and Ireland
ABG Arterial blood gas
ACE Angiotensin converting enzyme
Ach Acetylcholine
AChE Acetyl cholinesterase
ACS Acute coronary syndrome
ACTH Adrenocorticotrophic hormone
ADH Antidiuretic hormone
AF Atrial fibrillation
AHA American Heart Association
AKI Acute kidney injury
ALS Advanced life support
AMP Adenosine monophosphate
APTT Activated partial thromboplastin time
ATP Adenosine triphosphate
BIPAP Bilevel positive airways pressure
BMI Body mass index
BPM Beats per minute
CABG Coronary artery bypass graft
CAD Coronary artery disease
CCF Congestive cardiac failure
CNS Central nervous system
CO Cardiac output
CO2 Carbon dioxide
COPD Chronic obstructive pulmonary disease
CPAP Continuous positive airways pressure
CPET Cardiopulmonary exercise test
CRF Chronic renal failure
CSF Cerebrospinal fluid
CT Computed tomography
CVA Cerebrovascular accident
CVC Central venous catheter
CVP Central venous pressure
CVS Cardiovascular system
CXR Chest x-ray
DBP Diastolic blood pressure
DVT Deep venous thrombosis
ECG Electrocardiogram
ECT Electroconvulsive therapy
EDV End diastolic volume
EEG Electroencephalogram
EF Ejection fraction
EMG Electromyogram
ESA European Society of Anaesthesiology
ESC European Society of Cardiology
ETT Endotracheal tube
FBC Full blood count
FEV1 Forced expiratory volume in 1 second
FiO2 Inspired fraction of oxygen
FRC Functional residual capacity
FVC Forced vital capacity
GABA Gamma hydroxybutyric acid
GCS Glasgow comas scale
GFR Glomerular filtration rate
GH Growth hormone
GMP Guanosine monophosphate
GP General practitioner
GTN Glyceryl trinitrate
Hb Hemoglobin
HDL High-density lipoprotein
HDU High dependency unit
HIV Human immunodeficiency virus
HOCM Hypertrophic obstructive cardiomyopathy
I/E Inspired : expired ratio
IABP Intra-arterial blood pressure
ICP Intracranial pressure
ICU Intensive care unit
IG Immunoglobulin
IHD Ischemic heart disease
IM Intramuscular
IPPV Intermittent positive pressure
ventilation
IQ Intelligence quotient
IV Intravenous
JVP Jugular venous pressure
kPa Kilopascal
LBBB Left bundle branch block
List of abbreviations
LDL Low-density lipoprotein
LFT Liver function test
LM Laryngeal mask
LMA Laryngeal Mask Airway ™
LMN Lower motor neuron
MAC Minimum alveolar concentration
MAP Mean arterial pressure
MSH Melanocyte stimulation hormone
NICE National Institute of Health and Care Excellence
NIV Noninvasive ventilation
NMJ Neuromuscular junction
NO Nitric oxide
NREM Nonrapid eye movement
NSAID Nonsteroidal anti-inflammatory drug
NSTEMI Non-ST-elevation myocardial infarction
NYHA New York Heart Association
O2 Oxygen
P50 Partial pressure of oxygen at 50% saturation
PaO2 Arterial partial pressure of oxygen
PAC Pulmonary artery catheter
PaCO2 Arterial partial pressure of carbon dioxide
PAP Pulmonary artery pressure
PEEP Positive end-expiratory pressure
PEFR Peak expiratory flow rate
PET Positron emission tomography
PFT Pulmonary function test
PONV
Postoperative nausea and vomiting
PT Prothrombin time
PTH Parathyroid hormone
PTT Partial thromboplastin time
PVR Pulmonary vascular resistance
RBBB Right bundle branch block
REM Rapid eye movement
SaO2 Arterial saturation of oxygen
SAP Systolic arterial pressure
SLE Systemic lupus erythematosus
STEMI ST-elevation myocardial infarction
SVR Systemic vascular resistance
TB Tuberculosis
TIA Transient ischemic attack
TIVA Total intravenous anesthesia
TNF Tumor necrosis factor
TNM Tumor nodes metastases
TOE Transesophageal echocardiogram
TSH Thyroid stimulating hormone
TTE Transthoracic echocardiogram
U&E Urea and electrolytes
UK United Kingdom
UMN Upper motor neuron
USS Ultrasound scan
V/Q Ventilation : perfusion
VC Vital capacity
VF Ventricular fibrillation
VT Tidal volume
WHO World Health Organization
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Respiratory system
MATTHEW STAGG
ASTHMA
A very common respiratory disorder characterized by recurrent attacks of paroxysmal dyspnoea with reversible variable airflow obstruction and increased bronchial hyper-responsiveness to a range of stimuli. Aetiology, pathology and clinical presentation are heterogenous, but an underlying inflammatory response is usually present. There is an immense range of clinical pathology from children with reversible bronchospasm through to elderly patients in whom bronchospasm is superimposed on chronic respiratory disease. The incidence of intraoperative bronchospasm is low and tends to occur in older
asthmatics and those with active or poorly controlled asthma at the time of operation.
EPIDEMIOLOGY
Variable geographical distribution, affecting about 5% of the population as a whole but up to 10% of children.
MORBIDITY
Increased risk of postoperative respiratory complications, especially in the older patient with chronic airways disease in whom cardiac problems may also be present.
Histamine + + +
Prostaglandin + +
Leukotrienes
C4, D4, E4 + + +
Thromboxane + +
Platelet activating factor + +
PATHOPHYSIOLOGY
Nonspecific airway hyper-responsiveness is common. There is an increased response to methacholine, exercise, histamine, cold-air challenge, hyperventilation or extreme emotional stimulus. Airway obstruction is due to constriction of airway smooth muscle, mucus secretion and oedema of the airway wall. Mechanisms include neural and cellular pathway activation. The neural pathway involves afferent irritant receptors in airways, causing reflex stimulation of postganglionic parasympathetic fibres, resulting in smooth muscle constriction and mucus secretion. C fibre stimulation releases local neuropeptides; substance P changes membrane permeability and mucus secretion; neurokinin A causes bronchoconstriction. Cellular pathway activation involves immunoglobin E mediated histamine release from mast cells. Eosinophils, neutrophils, macrophages and lymphocytes CD8 and Th1 may also release mediators including leukotrienes, LTB4 and the cysteinyl leukotrienes, CysLT. LTB4 is a pro-inflammatory mediator with potent neutrophil chemotaxic properties while CysLTs are potent bronchoconstrictors that increase vascular permeability, cause mucus secretion, mucociliary dysfunction, stimulate eosinophil recruitment and increase bronchial responsiveness. At a cellular level, smooth muscle tone is controlled by intracellular cyclic AMP and possibly cyclic GMP, with lower levels leading to bronchoconstriction. The effect on ventilatory function can be extreme, with increased work of breathing, air trapping, exhaustion, hypercapnia and potentially fatal V/Q mismatch resulting in lifethreatening hypoxia. This may be sustained for several days.
PREOPERATIVE ASSESSMENT
Optimise treatment in consultation with a respiratory physician. Severity and frequency of attacks, hospital admissions, exercise tolerance, current medication and trigger factors are essential information. Frequency of inhaler use may inform about severity and stability of their asthma. Steroid use, time of last exacerbation, timing and duration of any hospital admission are important.
Factors that indicate increased propensity to bronchospasm include recent or current upper respiratory tract infection, steroid use and past history of respiratory complications related to surgery. Previous ICU admission, especially one requiring intubation and ventilation, should act as a ‘Red Flag’. In non–asthmatics, a family history of atopy or of asthma should alert to the possibility of intra-operative bronchospasm.
Some patients with COPD may have a significant reversible component. The presence of wheezes might indicate inadequate control and suggest medication review. The presence of a respiratory tract infection is a relative contraindication to anaesthesia.
INVESTIGATIONS
Chest X-ray – Look for hyperinflation; chronic lung changes or concomitant cardiac problems in older patients; evidence of right ventricular predominance, suggesting long-standing major problems.
ECG – Look for evidence of long-standing right ventricular hypertrophy or cor pulmonale. Such patients constitute a very high-risk group. Lung function tests – FEV1 reduced more than FVC (FEV1 normally 50 mL kg –1, and 70%–80% FVC). Blood gases – Useful in asthmatics with COPD to be used as a baseline to guide postoperative target goals.
MEDICATION
The range of agents that can maintain control of asthma is considerable (Table 1.1). Many are long acting. Patients should continue on their maintenance therapy throughout their hospital stay if possible. Preoperative management strategies.
Table 1.1 Agents used to maintain control of asthma
Drug type
Stabilizing agents
Bronchodilators
β2 agonist short-acting 4–6 h
β2 agonist long acting >12 h
Phosphodiesterases
Inhaled steroids
Inhaled anticholinergics
Leukotriene antagonists
IgE immunotherapy
Others
Gases
Example agents
Sodium chromoglycate
Salbutamol/levosalbutamol
Terbutaline
Arformeterol
Salmeterol
Aminophyline
Becotide, flixotide, budenoside
Ipratropium
Zileuton montelukast pranlukast
Omalizumab
Ketamine
Magnesium
Volatile agents
Heliox
Clinical Preoperative intervention
Asymptomatic Nothing needed
No medications
No recent asthma episodes
No obstruction on spirometry
Occasional bronchodilators
Probably nothing needed
No steroids Dose prior to induction suggested
Inhaled steroids Continue inhaled steroids
Give bronchodilator prior to induction
Spirometry below baseline Consider short course oral steroids
Oral steroids Continue same dose preoperatively
Consider extra dose at induction
Probable hydrocortisone postop for several days
PREMEDICATION
Sedation is useful as anxiety may provoke an attack in some patients. Atropine or glycopyrrolate inhibits vagally mediated bronchospasm but
Side effects
Tremor anxiety tachycardia
Hypokalaemia/hypomagnesaemia
Less side effects
No antiinflammatory action
Tachycardia/arrhythmias
Sympathomimetic
Smooth muscle relaxation
Bronchodilation
Reduced airway resistance
FiO2 < 1
produces tachycardia. Preoperative bronchodilators and steroids reduce the likelihood of postoperative complication, so consider an additional dose of bronchodilator by inhaler or nebulizer prior to induction. Patients on steroids should receive steroids and if on high doses (>1500 μg day –1 in adults; less in children) give peri- and postoperative replacement as adrenal suppression may be present. Neither wound healing nor infection problems are relevant with these short periods of increased steroid use.
CHOICE OF ANAESTHESIA
Regional anaesthesia is recommended but anxiety can trigger bronchospasm so patient acceptance is important. If general anaesthesia is necessary, avoid stimulation of the respiratory tract and drugs known to cause bronchospasm.
INDUCTION
Avoid agents that may release histamine. Thiopentone is safe although it can cause histamine release and does not block airway reflexes. Propofol has bronchodilator properties and suppresses airway reflexes. Etomidate is safe. Ketamine is suitable for induction and maintenance by infusion in the asthmatic patient with bronchospasm requiring emergency anaesthesia,
Respiratory system
although it may produce tachycardia and increased secretions. It may also be used to treat status asthmaticus. Sevoflurane is widely used and well tolerated.
INTUBATION
Spraying the larynx with lidocaine, prior to intubation, may help although it can itself stimulate bronchospasm (not histamine mediated). The use of a laryngeal mask avoids airway stimulation and the need for muscle relaxants. If control of hypercapnia, airway protection or emergency ventilation is required, an endotracheal tube is the only option.
MAINTENANCE
Halothane, enflurane, isoflurane and sevoflurane are all potent bronchodilators. They have been used in the treatment of refractory asthma and are ideal for maintaining anaesthesia.
MUSCLE RELAXANTS
Suxamethonium is a potent histamine releaser, so avoid if possible. Atracurium and mivacurium are associated with bronchospasm from histamine release. Pancuronium, vecuronium and cisatracurium appear safe while rocuronium has been associated with some severe reactions although in high does may be used as an alternative to suxamethonium. Reversal with anticholinesterases can trigger bronchospasm although atropine or glycopyrrolate given concurrently reduces the severity of this.
ANALGESIA
Local and regional techniques are recommended, but are not always feasible. Morphine and diamorphine release histamine and should be avoided. Pethidine has been widely used although may have some histamine-releasing potential. Fentanyl and alfentanil are safe. Exercise caution with NSAIDs unless previous exposure has not yielded problems.
POSTOPERATIVE MANAGEMENT
Problems in older asthmatics usually relate to underlying chronic lung disease. Effective analgesia assists
physiotherapy and coughing so preventing the development of atelectasis and concurrent infection. Warm, humidified air and bronchodilators minimize the impact of mucus retention and plugging.
THE EMERGENCY CASE WITH CURRENT SYMPTOMATIC BRONCHOSPASM
A potentially disastrous situation, but fortunately rare. Surgery must be absolutely life or limb threatening to warrant proceeding. If possible, use a regional technique. Treat bronchospasm aggressively with IV steroids, magnesium sulphate 2 gm IV and/or aminophylline IV. The induction agent of choice is ketamine, followed by ketamine infusion, although other induction agents are often used effectively and safely. Suxamethonium may release histamine but its use may be difficult to avoid, unless high dose rocuronium is an option. Fentanyl is recommended for analgesia. Inhalational agents (sevoflurane or halothane) are effective in treating bronchospasm. Once deep on these agents, the patient may be better controlled than prior to induction. Continued bronchospasm with high airway pressure may necessitate IV beta agonists or even epinephrine (nebulizer or intravenously) in extreme circumstances.
Ventilation may pose problems, as airway pressures are likely to be high. Manipulate tidal volume, rate and I/E ratio to minimize peak airway pressure but maintain adequate minute ventilation. Permissive hypercapnia is reasonably tolerated. The possibility of a pneumothorax must be continuously considered. Postoperative management should be in ICU.
DEVELOPMENT OF INTRAOPERATIVE ASTHMA
Not all wheezing is asthma. Tube contact with the carina or a main bronchus can produce wheezing. Airway obstruction may result from tube blockage, secretions or blood. Aspiration, tension pneumothorax, anaphylactic or anaphylactoid reaction may all produce bronchospasm.
Salbutamol (2–5 μ g kg –1) or aminophylline (5 mg kg –1) slow IV may be given. Steroids (e.g.
hydrocortisone) will not have an immediate effect but may assist in gaining control. Airway pressures may have been very high so beware of a pneumothorax.
The end of the case is a critical time when bronchospasm may appear in an awakening patient. Extubation deep may reduce the likelihood of bronchospasm but in many cases is inappropriate. Reversal with neostigmine can provoke bronchospasm but atropine or glycopyrrolate reduce the risk. Avoiding all reversal agents is ideal. Sugammadex may be a viable alternative.
DRUGS TO AVOID
Tubocurarine
Morphine, diamorphine and other histaminereleasing opiates
Beta blockers
Aspirin and other NSAIDs which are prostaglandin mediated
REFERENCES
Burburan SM, Xisto DG et al. (2007). Anaesthetic management in asthma. Minerva Anestesiol 73(6): 357–65.
Colebourn CL, Barber V et al. (2007). Use of helium-oxygen mixture in adult patients presenting with exacerbations of asthma and chronic obstructive pulmonary disease: A systematic review. Anaesthesia 62(1): 34–42.
Doherty GM, Chisakuta A et al. (2005). Anesthesia and the child with asthma. Paediatr Anaesth 15(6): 446–54.
Tirumalasetty J, Grammer LC. (2006). Asthma, surgery, and general anesthesia: A review. J Asthma 43(4): 251–4.
Woods BD, Sladen RN. (2009). Perioperative considerations for the patient with asthma and bronchospasm. Br J Anaesth 103 Suppl 1 : i57–65.
CROSS-REFERENCES
Intraoperative bronchospasm, Chapter 30
Ventilators, Chapter 27
BRONCHIECTASIS
Bronchiectasis is characterized by long-standing abnormal dilatation of bronchi with chronic inflammation. This chronic inflammatory process results in patients being extremely productive of sputum with a predisposition to either chronic infection or colonisation with intermittent acute episodes of infection.
Historically bronchiectasis was a consequence of chronic recurrent infection. Pneumonias, measles, whooping cough, TB and fungal infections were the main causes. Now with antibiotics, vaccination and better nutrition it is far less common. Cystic fibrosis and smoking are now the main causes. Sometimes patients will present for surgical treatment of their bronchiectasis. There are some specific associated syndromes including Kartageners (the combination of situs inversus, sinusitis and bronchiectasis).
Diagnosis is by high-resolution CT scan and anaesthesia for bronchography has been relegated to history.
PATHOPHYSIOLOGY
Following childhood pneumonia or recurrent adult infections.
Congenital:
– Cystic fibrosis
– Bronchial cartilage deficiency
– Abnormal ciliary motility (Kartageners)
– Hypogammaglobulinaemia
Distal to bronchial obstruction:
– Inhaled foreign body
– Tumour
Clinical features are variable. In severe bronchiectasis there is up to 500 mL of purulent sputum per day, which gets dramatically worse during an acute exacerbation. Other features include haemoptysis from areas of severe inflammation with altered local circulation arising from bronchial and intercostal arteries. In long-standing disease pulmonary hypertension and cor pulmonale may develop. Metastatic abscess formation can occur. Amyloidosis is a rare complication.
MANAGEMENT
Chest physiotherapy with percussion and postural drainage is key but early intervention with antibiotics may prevent acute exacerbations. These patients are often chronically colonised with resistant organisms due to frequent antibiotic exposure. Pseudomonas aeruginosa and Haemophilus influenzae are particularly common.
PREOPERATIVE ASSESSMENT
Exercise tolerance (compared with their usual state), sputum production and frequency of acute exacerbations predict the severity. Information about colonising organisms and antibiotic history are important.
INVESTIGATIONS
Blood gases – To determine present baseline, and to guide postoperative target goals.
Chest X-ray – Probably not of benefit. A recent CT scan is helpful.
Pulminary function tests – Generally not very helpful. ECG – Look for signs of right ventricular strain or cor pulmonale.
Echocardiogram – Helpful in assessing right ventricular hypertrophy, myocardial function and raised pulmonary pressures.
PREOPERATIVE MANAGEMENT
The patient will need extensive physiotherapy and be exacerbation free prior to surgery. Discussion with chest physician and microbiologist should determine the appropriate antibiotic to use preoperatively.
ANAESTHETIC MANAGEMENT
The surgery will determine the most appropriate form of anaesthesia. If possible, use regional techniques. Use routine monitoring commensurate with the anaesthetic and surgery. Have a very low threshold for an arterial line. There are no particular agents that are contraindicated. Try to keep the oxygen saturations high (>90%) to maintain a safety margin. End tidal CO2
is likely to be different from the arterial value but should provide trend measurements.
Sputum retention is likely to be a problem and will predispose to secondary infection. Humidify all gases and persist with regular tracheal suction. It may be necessary to use a bronchoscope to remove inspissated secretions and sputum. In cases with very severe localised bronchiectasis, it may be feasible to try to isolate that part of the lung with a bronchial blocker. Proper attention to sterile technique is important, particularly in those with Kartageners syndrome as they also have a defect in neutrophil chemotaxis. Nasal tubes should be avoided in view of the accompanying sinusitis.
POSTOPERATIVE CARE
Arrange early postoperative physiotherapy in advance. In cases of cystic fibrosis, HDU care may be helpful to ensure mobilization and physiotherapy. Good analgesia is essential and patient-controlled devices, epidural analgesia or NSAIDs are all useful. Entonox may be helpful. Avoid postoperative ventilation wherever possible.
REFERENCES
Gavai M, Hupuczi P et al. (2007). Spinal anesthesia for cesarean section in a woman with Kartagener’s syndrome and a twin pregnancy. Int J Obstet Anesth 16(3): 284–7.
Howell PR, Kent N et al. (1993). Anaesthesia for the parturient with cystic fibrosis. Int J Obstet Anesth 2(3): 152–8.
Lamberty JM, Rubin BK. (1985). The management of anaesthesia for patients with cystic fibrosis. Anaesthesia 40(5): 448–59.
Yim CF, Lim KS et al. (2002). Severe pulmonary hypertension in a patient with bronchiectasis complicated by cor pulmonale and a right-to-left shunt presenting for surgery. Anaesth Intensive Care 30(4): 467–71.
Hopkin JM. (1987). The suppurative lung diseases.
In: Weatherall D J, Ledingham J G G, Warrell D A (eds.). Oxford Textbook of Medicine, 2nd edn. Oxford University Press, Oxford, pp. 15.100–15.103.
Katz J. (1998). Anaesthesia and Uncommon Diseases 5th edn. W B Saunders, Philadelphia.
CROSS-REFERENCES
Preoperative assessment – specific medical problems, Chapter 25
Cardiopulmonary exercise testing, Chapter 25
BRONCHOGENIC CARCINOMA
Lung cancer is the most common cause of cancer mortality worldwide for men and women, causing approximately 1.2 million deaths per year (Table 1.2). The most common symptoms are unexplained persistent cough, haemoptysis, shortness of breath, chest pain, bone pain and weight loss. They may develop from airways or parenchyma.
The main types are non-small cell lung carcinoma (NSCLC) and small cell lung carcinoma (SCLC). Early stage (stage 1–2) NSCLC is treated with surgery, while SCLC is treated by chemotherapy and radiation. Other tumours including large cell, neuroendocrine (carcinoid), bronchioloalveolar and rarer forms can all present as lung malignancies. The most common cause is long-term exposure to tobacco smoke. Lung cancer in non-smokers (15% of cases) is often attributed to a combination of genetic factors, radon gas, asbestos, air pollution and passive exposure to cigarette smoke.
Derived from the epithelium, squamous cell carcinomas are the most common NSCLC. They are usually centrally located at the carina or in the 1–3rd generation bronchi. Adenocarcinoma is less common with peak incidence in men in their fifties.
Presentation includes airway obstruction, lung collapse, and distal infection or through spread via the peribronchial tissues with subsequent invasion of the mediastinum. It spreads by both lymphatic and haematological routes and distal metastasis is common in liver, adrenals, bone and brain.
All forms of treatment can be associated with notable toxicity. Patients with significant impairment due to their lung cancer or comorbid conditions may not be fit to undergo resection or even aggressive chemoradiotherapy. Performance status can be assessed by a variety of methods including the Karnofsky Performance Status (KPS) or the World Health Organisation (WHO) status.
Anaesthetic involvement is mainly for lung resection (e.g. lobectomy, pneumonectomy). However, newer indications for palliative interventional bronchoscopic procedures are increasing. Debulking/ disobliteration of central symptomatic obstructive lesions followed if necessary by tracheobronchial stents can ameliorate some symptoms of advancing disease. This may be done by rigid or flexible bronchoscopy, using a number of different modalities such as electrocautery, laser, cryotherapy/ cryoextraction, argon plasma coagulation or mechanical debulking.
PREOPERATIVE ASSESSMENT
Patients may be asymptomatic or may present with a range of symptoms and signs including:
Local – Chest pain, cough, dyspnoea, haemoptysis, hoarseness, pleural effusion. Distal – Metastases with associated problems. Other – Ectopic hormonal activity from paraneoplastic tumours (e.g. ACTH, PTH, ADH, insulin and glucagon). Some manifestations of Cushing’s syndrome can occur with hypokalaemia although the full clinical features of Cushing’s syndrome are rarely seen as they do not have time to develop. Lambert–Eaton syndrome has been reported. Serotonin secreting adenomas may present as episodic sweating, wheeze and
Table 1.2 Lung cancer and its incidence
Respiratory system breathlessness. These patients are usually smokers and COPD is a common concomitant problem.
INVESTIGATIONS
• Chest X-ray – May not reveal the tumour but may show signs of concomitant problems such as COPD. A pleural effusion or pericardial effusion would suggest mediastinal invasion.
• ECG – Thoracic surgery can result in rhythm disturbance, especially atrial fibrillation. Smokers have a high incidence of asymptomatic heart disease.
• Electrolytes – May indicate ectopic ADH secretion with low sodium which will eventually produce clinical signs of confusion and weakness. Ectopic ACTH secretion can result in hypokalaemia or hyperkalaemia with or without hypernatraemia. PTH produces hypercalcaemia but so do widespread bony metastases with elevated alkaline phosphatase. Glucose values can be adversely influenced by ectopic insulin or glucagon.
• Lung function tests – Important if any significant lung resection is planned. FEV1 and FVC are most useful, whilst low gas transfer (below ~30%) may have implications for risk of postoperative respiratory failure. CPET may be helpful and baseline arterial blood gases on air should be taken.
Patients will have likely presented through a lung multidisciplinary team. A chest CT and or CT-PET scan, and tissue sampling by bronchoscopy, transbronchial needle aspiration, mediastinoscopy or interventional radiology will have staged the disease enabling appropriate management.
INOPERABILITY
The TNM staging system of the international union against lung cancer (Table 1.3) will determine which primary lung cancers are theoretically operable. In general, stage 1 and 2 disease is operable. Some classical indicators of inoperability exist which
indicate stage 3 or 4 advanced disease. These include SVC obstruction or other great vessel involvement, nerve palsies including left recurrent laryngeal and phrenic nerve damage, carinal or tracheal involvement, oesophageal invasion, vertebral involvement and Pancoast’s syndrome.
Pancoast’s syndrome is an apical carcinoma invading the eighth cervical and first thoracic nerves. Severe pain and wasting in the upper limbs occur with stellate ganglion involvement. The patient often has Horner’s syndrome (ptosis, enophthalmos, miosis, impaired sweating on face).
Very often these patients have palliative stents placed for debulked endobronchial disease or symptomatic compressive extrinsic disease. They can be silicon or metallic-nitinol alloy (placed via rigid bronchoscopy or interventional radiology) requiring general anaesthesia. Nitinol bronchial stents can be placed via flexible bronchoscopy under general anaesthesia or conscious sedation, or through endobronchial tubes. Complications include migration, misplacement, infection, biofouling and stent fractures (in older generation stents). These procedures usually offer immediate relief of symptoms and at least short-term benefit in the acute setting. They have even been attributed to liberation from mechanical ventilation after acute respiratory failure.
PREOPERATIVE PREPARATION
Optimize respiratory function – beta 2-adrenergic agonists, anticholinergics, active physiotherapy and steroids as indicated.
Any sizeable effusions should be drained. Electrolytes and haemoglobin should be corrected. While a restrictive approach to transfusion should be adopted, these patients are at risk of ischaemic heart disease so aim for Hb > 10 g/dL.
In patients having debulking techniques or stenting, careful consideration of anatomical placement of the stent should be discussed with the operator prior to anaesthesia. Modern imaging provides useful information that often correlates with functionality. Patients will often be dyspnoeic and may have partially collapsed lung segments. They are usually dramatically improved by the procedure but if the collapse has been long-standing it may be
Table 1.3 TNM staging system for lung cancer (7th edition)
Primary tumour (T)
T1
Tumour ≤3 cm diameter, surrounded by lung or visceral pleura, without invasion more proximal than lobar bronchus
T1a Tumour ≤2 cm in diameter
T1b Tumour >2 cm but ≤3 cm in diameter
T2
Tumour >3 cm but ≤7 cm, or tumour with any of the following features:
Involves main bronchus, ≥2 cm distal to carina
Invades visceral pleura
Associated with atelectasis or obstructive pneumonitis that extends to the hilar region but does not involve the entire lung
T2a Tumour >3 cm but ≤5 cm
T2b Tumour >5 cm but ≤7 cm
T3 Tumour >7 cm or any of the following:
Directly invades any of the following: chest wall, diaphragm, phrenic nerve, mediastinal pleura, parietal pericardium, main bronchus <2 cm from carina (without involvement of carina)
Atelectasis or obstructive pneumonitis of the entire lung
Separate tumour nodules in the same lobe
T4 Tumour of any size that invades the mediastinum, heart, great vessels, trachea, recurrent laryngeal nerve, oesophagus, vertebral body, carina, or with separate tumour nodules in a different ipsilateral lobe
Regional lymph nodes (N)
N0 No regional lymph node metastases
N1
N2
N3
Distant metastasis (M)
Metastasis in ipsilateral peribronchial and/or ipsilateral hilar lymph nodes and intrapulmonary nodes, including involvement by direct extension
Metastasis in ipsilateral mediastinal and/or subcarinal lymph node(s)
Metastasis in contralateral mediastinal, contralateral hilar, ipsilateral or contralateral scalene, or supraclavicular lymph node(s).
M0 No distant metastasis
M1 Distant metastasis
M1a
Separate tumour nodule(s) in a contralateral lobe; tumour with pleural nodules or malignant pleural or pericardial effusion
M1b Distant metastasis
Stage groupings
Stage IA
Stage IB
Stage IIA
Stage IIB
Stage IIIA
Stage IIIB
Stage IV
T2a
T1a,T1b,T2a
T2b
T2b
T3
T1a,T1b,T2a,T2b
T3
T4
T4
Any T
Any T
Respiratory system
irrecoverable and predispose to infection. Careful planning is required.
PREMEDICATION
Minimise stress to the patient with an anxiolytic if necessary. A drying agent may help.
ANAESTHETIC TECHNIQUE
In patients with tracheal or bronchial compromise, coughing may become problematic and threaten airway patency. Inhalational techniques are likely to precipitate problems. General anaesthesia with muscular relaxation and mechanical ventilation is usually required. Almost any induction technique is suitable. Short- to medium-acting relaxants which do not accumulate are ideal with neuromuscular monitoring. Volatile agents are bronchodilators. Some advocate the use of heliox during induction if there is significant airway narrowing. Remifentanil has been recommended.
For lung resection, a double lumen endotracheal tube allows single lung ventilation and optimises surgical field. Alternatively an endobronchial blocking balloon may be placed under bronchoscopic vision.
Partial or complete central airway obstruction or symptomatic trachea-broncho-oesophageal fistulae can sometimes be palliated by debulking and/ or stenting, respectively. Stents require appropriate and careful planning regarding position, size and type. Bronchial stents may be deployed awake or under general anaesthesia. Rigid bronchoscopy with a Sanders injector is a well-established technique, as is the suspension laryngoscope. Remember that the Sanders injector can result in high pressure air trapping if there is partial obstruction. Adequate neuromuscular reversal is vital prior to extubation. At the end of the case ensure there is a good cough reflex.
PATIENTS WITH PREEXISTING STENTS NEEDING ANAESTHESIA
Ensure the stent position is known, image if possible, seek an opinion from whoever placed the stent and ideally view the stent bronchoscopically prior to intubation The aim is to avoid dislodging the stent. In an emergency, try to visualise it before intubation if possible.
ACUTE POSTOPERATIVE CENTRAL AIRWAY OBSTRUCTION
It may be difficult to reestablish spontaneous breathing. The appearance has been likened to inadequate neuromuscular reversal with an ineffective breathing pattern that is largely abdominal. Desaturation ensues often associated with a deteriorating level of consciousness which may be in part due to hypercarbia. Blood gases show hypercarbia and hypoxia. Assume airway obstruction. Control the airway and with the aid of a surgeon go to rigid bronchoscopy as secretions at the carina or in the trachea are the most likely cause. The differential diagnosis is tension pneumothorax after airway instrumentation but that is very rare from stent placement in experienced hands.
POSTOPERATIVE CARE
This depends on the nature of the surgery, requirement for ventilation, preoperative respiratory function and other co-morbidities. Even without ventilation, these patients will often require specialist postoperative care. Epidurals, oral opioids and PCA are most commonly used for analgesia. Pain will impair chest movement so good analgesia is key to recovery.
Conacher ID. (2003). Anaesthesia and tracheobronchial stenting for central airway obstruction in adults. Br J Anaesth 90(3): 367–74.
Goldstraw P, Crowley J, Chansky K et al. (2007). The IASLC Lung Cancer Staging Project: Proposals for the revision of the TNM stage groups in the forthcoming (seventh) edition of the TNM classification of malignant tumours. J Thorac Oncol 2: 70.
Jones C, Crerar-Gilbert AJ, Madden BP. (August 2009). Anaesthesia for endobronchial intervention and tracheobronchial stents. Curr Anaesth Crit Care 20(4): 160–3.
O’Neill JH, Murray NM, Newson-Davis J. (1988). Lambert–Eaton Syndrome. A review of 50 cases. Brain III: 577–96.
Ramnath N, Demmy TL et al. (2007). Pneumonectomy for bronchogenic carcinoma: Analysis of factors predicting survival. Ann Thorac Surg 83(5): 1831–6.
Small S, Ali HH, Lennon VA, Brown RH, Carr DB, De Armendi A. (1992). Anesthesia for an unsuspected Lambert–Eaton myasthenic syndrome with autoantibodies and occult small cell lung carcinoma. Anesthesiology 76: 142–5.
CROSS-REFERENCES
Lobectomy, Chapter 15
Pneumonectomy, Chapter 15
One lung anaesthesia, Chapter 28
Intraoperative bronchospasm, Chapter 30
Preoperative assessment of pulmonary risk, Chapter 25
Cushings syndrome, Chapter 6
Myasthenia, Chapter 3
CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD)
A common chronic inflammatory disease of the lungs, there is a spectrum associated with expiratory airflow obstruction including emphysema and chronic bronchitis. It has pulmonary and systemic manifestations. Management guidelines are well established with evidence-based recommendations for chronic disease and acute exacerbations.
In 1990, COPD was ranked 12th as a burden of disease by the WHO; by 2020 it is projected to rank 5th. Cigarette smoking is its primary cause and up to 25% of smokers are likely to develop COPD.
Respiratory disease accounts for more than 25% of acute hospital admissions, of which more than half are acute exacerbations of COPD. Hospitalization carries up to 26% mortality, rising to 66% within 2 years.
The prevalence of COPD is 5%–10% among general surgical patients, 10%–12% in cardiac surgery and 40% in thoracic surgery as compared to 5% in the general population.
The pulmonary component of COPD is characterised by expiratory airflow limitation that is not fully reversible. The diagnosis, severity assessment
and monitoring rely heavily but not exclusively on spirometry. In smokers, lung function decline is accelerated beyond the natural 20–30 mL annual loss.
Airflow limitation is usually progressive and associated with an abnormal inflammatory response of the lung. Respiratory failure in COPD may be type 1 (predominantly hypoxic) or type 2 (associated hypercapnia). Chronic respiratory failure is often related to chronic hypoventilation, and may lead to cor pulmonale if untreated.
Patients with COPD, particularly severe disease, are at significant risk of postoperative complications. Preoperative recognition and optimisation can reduce these risks.
PATHOPHYSIOLOGY
Inflammatory small airways disease, destruction of alveolar units, inflammatory bronchiolitis and excess mucus production lead to airflow obstruction. Airways are no longer held open due to reduced elasticity and tone of the parenchyma. The combination of airway collapse prior to full emptying, bronchospasm and secretions produces expiratory airflow limitation and gas trapping. Loss of alveolar units decreases gas transfer.
An early manifestation is an increase in residual volume. The natural history is progressive gas trapping with decreasing vital capacity (VC). This results in a decline in forced expiratory volume in 1 second (FEV 1), further exacerbated by rapid shallow breathing, which leads to dynamic hyperinflation (Figure 1.1).
This increase in work of breathing is in part responsible for dyspnoea and exercise limitation. Due to differential transluminal pressures within the small conducting airways and at the alveolar level, lung units have different time constants for emptying. Across the whole lung, this results in retained intrathoracic pressure and so called ‘intrinsic PEEP’. In the longer term, an increase in residual volume and chronic hyperinflation with reduced efficiency of resting diaphragm position and function results. In those with chronic carbon dioxide retention, there is a predisposition to developing pulmonary hypertension and right heart failure (cor pulmonale). Associated conditions are malnutrition, musculoskeletal disorders, cardiovascular disease,
Expiration
Incomplete emptying
Increased residual volume
Intrinsic PEEP
Increased pressure on bronchiole from increased intrathoracic pressure
Secretions
Loss of rigidity in wall
Less elasticity
Collapsing bronchioles
Transmural pressure favours collapse
Hyperinflated chest wall
Reduced respiratory excursion
Cor pulmonale
Pulmonary hypertension
Active forced expiration
Flat less efficient diaphragm
diabetes and depression. Reduced weight, peripheral muscle strength and chronic sputum production portend a worse prognosis.
Ultimately, the final common pathway of decreased gas transfer, alveolar hypoventilation and respiratory muscle disadvantage produces ventilation/ perfusion mismatch (V/Q) resulting in hypoxaemia and/ or hypercarbia.
There is no clear correlation between lung function and blood gas features. Patients with hyperinflation, and resting tachypnoea, often have low arterial oxygen tensions and low gas transfer, but do not retain carbon dioxide on increasing oxygen therapy – these tend to be the emphysema spectrum patients. Conversely, it is the chronic bronchitic patients who tend to hypoventilate, are comfortable at rest, have chronic ventilatory failure with stable hypercapnia, but better spirometry, less gas trapping and preserved gas transfer that are at risk of hypercapnic narcosis with high inspired oxygen levels.
PREOPERATIVE ASSESSMENT
The risk of postoperative pulmonary complications and postoperative respiratory failure is high while
lesser complications such as atelectasis or infection are common.
• Symptoms of sleep disordered breathing (excessive daytime sleepiness or tiredness, snoring and witnessed apnoeas).
EXAMINATION
Look for:
• Hyperinflation
• Right heart dysfunction
• Incipient infection in the oropharynx
• Wheezes or rhonchi (correlate with complications so consider bronchodilators or steroids to eliminate wheezing)
• Ischaemic heart disease
Figure 1.1 Respiratory effects of COPD during expiration.
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The Project Gutenberg eBook of Journal of a second expedition into the interior of Africa, from the Bight of Benin to Soccatoo
This ebook is for the use of anyone anywhere in the United States and most other parts of the world at no cost and with almost no restrictions whatsoever. You may copy it, give it away or re-use it under the terms of the Project Gutenberg License included with this ebook or online at www.gutenberg.org. If you are not located in the United States, you will have to check the laws of the country where you are located before using this eBook.
Title: Journal of a second expedition into the interior of Africa, from the Bight of Benin to Soccatoo
To which is added, the journal of Richard Lander from Kano to the sea-coast, partly by a more eastern route.
Author: Hugh Clapperton
Contributor: Sir John Barrow
Samuel Clapperton
Richard Lander
Abraham V. Salamé
Release date: October 26, 2023 [eBook #71961]
Language: English
Original publication: London: John Murray, 1829
Credits: Galo Flordelis (This file was produced from images generously made available by The Internet Archive)
*** START OF THE PROJECT GUTENBERG EBOOK JOURNAL OF A SECOND EXPEDITION INTO THE INTERIOR OF AFRICA, FROM THE BIGHT OF BENIN TO SOCCATOO ***
London, Published Decr 1,
Painted by Gildon Manton. Engraved by Thos Lupton.
CAPTN HUGH CLAPPERTON, R N
1828, by John Murray, Albemarle Street
J O U R N A L OF
A
S E C O N D E X P E D I T I O N INTO THE INTERIOR OF AFRICA, FROM
T H E B I G H T O F B E N I N T O S O C C A T O O .
BY THE LATE COMMANDER CLAPPERTON, OF THE ROYAL NAVY
TO WHICH IS ADDED, THE JOURNAL OF RICHARD LANDER FROM KANO TO THE SEA-COAST, PARTLY BY A MORE EASTERN ROUTE WITH A PORTRAIT OF CAPTAIN CLAPPERTON, AND A MAP OF THE ROUTE, CHIEFLY LAID DOWN FROM ACTUAL OBSERVATIONS FOR LATITUDE AND LONGITUDE
LONDON: JOHN MURRAY, ALBEMARLE-STREET.
MDCCCXXIX
CHAPTER I
Journey from Badagry over the Kong mountains to the city of Eyeo or Katunga 1
CHAPTER II.
Residence at Eyeo, or Katunga, the capital of Youriba 38
CHAPTER III.
Journal of proceedings from Katunga, or Eyeo, to Boussa, on the Niger, or Quorra, the place where Mungo Park perished
CHAPTER IV.
Journey from Boussa, across the ferry of the Quorra, by Guarri and Zegzeg, to the city of Kano
CHAPTER V.
Journey from Kano to the camp of Bello, and from thence to Soccatoo
CHAPTER VI
Residence at Soccatoo, till the death of the author
LANDER’S JOURNAL.
APPENDIX.
A LIST, OR SUMMARY ACCOUNT, OF THE LATE CAPTAIN CLAPPERTON’S ARABIC PAPERS, TRANSLATED BY MR A V SALAME
No I (A description of the course of the river Cówara, . . .) 329
No. II. Translation of the Account of the “Expedition of Forty Christians,” &c. &c. 333
No III A Geographical Account of the Country, Rivers, Lakes, &c from Bornou to Egypt, &c 335
Nos. IV. to IX. Traditional Account of different Nations of Africa, &c. 337 A VOCABULARY OF THE YOURRIBA TONGUE FELLATAH
MAPS
Chart of the Route
The course of the Kowara or Quarra as described by Bello’s Schoolmaster.
SHORT SKETCH OF THE L I F E O F C A P T A I N C L A P P E R T O N.
BY LIEUTENANT-COLONEL CLAPPERTON
C H C was born in Annan, Dumfriesshire, in the year 1788. His grandfather, Robert Clapperton, M.D., was a man of considerable knowledge, as a classical scholar, and in his profession. He first studied at Edinburgh; but as, in those days, the continental colleges were considered superior in medicine and surgery, he went to Paris, and there studied for some time. On his return to his native country, he married Elizabeth Campbell, second cousin of Colonel Archibald Campbell of Glenlyon; and soon after settled in Dumfries-shire, at a place called Crowden Nows, where he remained until George Clapperton (the father of our traveller), and another son were born. He afterwards removed to Lochmaben, where he had an increase to his family of four sons and one daughter. All the sons became medical men, except the youngest and the only survivor, who entered his Majesty’s service, in the beginning of 1793, as a second lieutenant of marines. His eldest son, George Clapperton, married young to a daughter of John Johnstone, proprietor of the lands of Thorniwhate and Lochmaben Castle, and settled in Annan, where he was a considerable time the only medical man of repute in the place, and performed many operations and cures which spread his fame over the borders of England and Scotland. His father bestowed a good education upon him, which proved so useful a passport to public favour, that he might have made a fortune; but, unfortunately, he was, like his father, careless of money. He married a second wife, and was the father of no fewer than twenty-one children. Of the fruit of the first marriage,
he had six sons and one daughter who grew to men and women’s estate. All the sons entered his Majesty’s service, the youngest of whom was Captain Clapperton, the African traveller, and the subject of this memoir. In his person he resembled his father greatly, but was not so tall by two inches, being five feet eleven inches; had great breadth of chest and expansion of shoulders, and otherwise proportionably strong; and was a handsome, athletic, powerful man. He received no classical education, and could do little more than read and write, when he was put under the tuition of Mr. Bryce Downie, a man of general knowledge, but chiefly celebrated for his mathematical abilities. He remained with Mr. Downie until he required a knowledge of practical mathematics, including navigation and trigonometry. He was found an apt scholar and an obliging boy by Mr. Downie, whose attention was never forgot by the traveller; as he expressed a great wish, when he arrived the first journey from Africa, that he could have had time to see his native country, and shake his old master once more by the hand. Captain Clapperton left Mr. Downie about the age of thirteen; when, by his own wish, he was bound an apprentice to the owner of a vessel of considerable burthen, trading between Liverpool and North America. After making several voyages in that vessel, he either left her, or was impressed into his Majesty’s service, and was put on board a Tender then lying at Liverpool, which vessel carried him round to Plymouth, where he with others were draughted on board of his Majesty’s ship Gibraltar, of eighty guns. He did not remain long in that ship, as in 1806 he arrived at Gibraltar in a naval transport; from which he was impressed, with others, on board his Majesty’s frigate Renommée, Captain Sir Thomas Livingston. Opportunely for our traveller, at that time his Majesty’s ship Saturn, Captain Lord Amelias Beauclerc (belonging to Lord Collingwood’s fleet off Cadiz), arrived for the purpose of watering and refitting; and our traveller, learning that his uncle (now Lieut.-Col. Clapperton) was captain of royal marines on board the Saturn, sent him a letter describing his situation in the Renommée. The uncle having been an old messmate of Sir Thomas’s, when both were lieutenants at the Cape of Good Hope many years before, made it his business immediately to see Sir Thomas; and, through his intercession, Sir Thomas very kindly put
our traveller, for the first time, upon the quarter-deck as a midshipman. The Renommée very soon after left Gibraltar for the Mediterranean; and, when on the coast of Spain, had occasion to send boats to attack some enemy’s vessels on shore. Clapperton, being in one of the boats, was slightly, as he considered it, wounded in the head, which, however, afterwards gave him much annoyance. He remained in the Renommée, with Sir Thomas, until she returned to England, and was paid off, in the year 1808. He then joined his Majesty’s ship Venerable, Captain King, in the Downs, as a midshipman, where he did not remain long, having heard that Captain Briggs was going to the East Indies in the Clorinde frigate, and wishing to go to that country, he applied for his discharge, that he might enter with Captain Briggs; but he could not accomplish it before the Clorinde had sailed from Portsmouth; he was ordered, however, (by the admiral) to have a passage in a ship going to the East Indies. In the course of the voyage, they fell in with a ship in great distress, it then blowing a gale of wind; but humanity required assistance, if it could be given. A boat was ordered to be got ready, and Clapperton to go in her. He declared to his messmates his decided opinion that the boat could not possibly live in the sea that was then running, but that it was not for him to question the orders of his superior officer. On pushing off, he told his messmates to share equally among them any articles belonging to him, and bade them good bye. The boat had scarcely put off from the ship when she swamped, and as no assistance could be rendered, all hands perished, with the exception of two; one of whom was Clapperton, who, under such trying circumstances, encouraged and assisted his only surviving companion till his own strength failed him. Among others, he had previously struggled hard to save a warrant officer; but finding himself nearly exhausted, he was obliged to desist, and he perished. They then dropped off, one after the other, until the bowman and Clapperton were the only two remaining out of the whole boat’s crew The latter then made use of a common sea expression to the bowman, “Thank God, I am not the Jonah!” meaning that he was not, by his bad conduct in life, the cause of the Almighty visiting them with his vengeance. The bowman seconded him in the exclamation, and they kept cheering each other until the
gale so far abated, that another boat was got out and sent to their relief.
They then proceeded upon their voyage; and in March, 1810, Clapperton joined his majesty’s ship Clorinde, where he received the greatest attention from Captain Briggs during the time he was on board. In 1812, when lying in Bombay harbour, he was joined by another messmate, the Hon. F. Mackenzie, youngest son of the late Lord Seaforth, between whom a most sincere friendship was contracted. Not long after this, Mr. Mackenzie was attacked with a severe illness, on which occasion Clapperton never left him, but nursed him as he would his own brother, until he died; when he added a lock of his hair to his locket, which contained that of his father and some friends. He returned to England in the end of 1813, or beginning of 14; and he was then sent, with some other intelligent midshipmen, to Portsmouth dock-yard, for the purpose of being instructed in Angelo’s sword exercise, in which he afterwards excelled. When these midshipmen were distributed to the different ships in the fleet as drill-masters, Clapperton volunteered his services for the Canadian lakes, and was sent on board Sir Alexander Cochrane’s flag ship, the Asia. This ship continued at Spithead till the end of January, 1814. During the passage to Bermudas, Clapperton’s services as a drill were performed on the quarter-deck. On her arrival, he was sent to Halifax, and from thence to the lakes, just then about to become the scene of warlike operations. During his passage out and his stay at Bermuda, nothing could exceed his diligence in the discharge of his duty with the officers and men. At his own and the other mess-tables, he was the soul and life of the party: he could sing a good song, tell humorous tales, and his conversation was extremely amusing. He bade adieu to all on board the Asia, and pursued his voyage to Halifax; from that to Upper Canada.
Soon after he arrived on the lakes, in 1815, he was placed in a situation that strongly marked that benevolence which was so strong a feature in his character. In the winter he was in command of a blockhouse on Lake Huron, with a party of men, for the purpose of defending it: he had only one small gun for its defence; he was
attacked by an American schooner; the blockhouse was soon demolished by the superiority of the enemy’s fire; and he found that himself and the party must either become prisoners of war, or form the resolution of immediately crossing Lake Michigan upon the ice, a journey of nearly sixty miles, to York, the capital of Upper Canada, and the nearest British depot. Notwithstanding the difficulty and danger attending a journey of such length over the ice in the depth of winter, the alternative was soon adopted, and the party set out to cross the lake, but had not gone more than ten or twelve miles, before a boy, one of the party, was unable to proceed from the cold; every one of the sailors declared that they were unable to carry him, as they were so benumbed with the cold, and had scarcely strength sufficient to support themselves. Clapperton’s generous nature could not bear the idea of a fellow-creature being left to perish under such appalling circumstances, for a dreadful snow-storm had commenced; he therefore took the boy upon his back, holding him with his left hand, and supporting himself from slipping with a staff in his right. In this manner he continued to go forward for eight or nine miles, when he perceived that the boy relaxed his hold; and on Clapperton examining the cause, he found that the boy was in a dying state from the cold, and he soon after expired. The sufferings of the whole party were great before they reached York; the stockings and shoes completely worn off their feet; their bodies in a dreadful state from the want of nourishment, they having nothing during the journey except one bag of meal. From the long inaction of Clapperton’s left hand, in carrying the boy upon his back, he lost, from the effects of the frost, the first joint of his thumb.
Not long after this, Sir Edward Owen was appointed to the command upon the lakes. A short time after his arrival, he gave to Clapperton an acting order as a lieutenant, and appointed him to the Confiance. While belonging to this ship, he often made excursions on shore, with his gun, into the woods, for the purpose of getting a little fresh meat. In these excursions he cultivated an acquaintance with the aborigines of the forest, and was much charmed with their mode of life. He had sent to his uncle in England the acting order which Sir Edward Owen had given him, that it might be laid before the Board of Admiralty for their confirmation; but, unfortunately, a
very large promotion had taken place a little before his acting order came to England, and the Board declined confirming his commission. No sooner was he made acquainted with its ill success, than he formed the idea of quitting his Majesty’s service altogether, and becoming one of the inhabitants of the North American forests. Fortunately for him, he some time afterwards abandoned that idea.
While the Confiance was at anchor near the shores of the Lake, Clapperton often went on shore to dinner and other parties. When he thought it time to return on board, he never employed a boat; being an expert swimmer, he plunged into the water with his clothes on, and swam along-side of the vessel; but this mode of proceeding very nearly lost him his life. One night he was so exhausted, that he could scarcely make the people on board hear his cries: they got a boat ready, and, as he was on the point of sinking, they picked him up, and took him on board; but he never tried the same method of getting on board again.
About the end of 1816, Sir Edward Owen returned to England, and was the means of Clapperton’s commission being confirmed by the Board of Admiralty And in the year 1817, when our vessels on the Canadian lakes were paid off and laid up, Lieutenant Clapperton returned to England, and, like many more, was put on half-pay. He went then to Edinburgh, where he remained a short time, and was introduced to the amiable mother of his beloved friend, Mr. Mackenzie, who died at Bombay. He afterwards retired to Lochmaben in 1818, and lived with an aged sister of his beloved mother’s, at the abode for many years of his grandfather. Here he continued to amuse himself with rural sports until 1820, when he went to Edinburgh, and there became acquainted with Dr Oudney, who mentioned to him the offer that had been made to employ him in a mission to the interior of Africa. This was an opening, to Clapperton’s enterprising mind, not to be resisted; he immediately entreated that he might accompany the doctor, and his offer was accepted. Dr. Oudney was told by a friend that knew Lieutenant Clapperton well, that, in all varieties, and under every circumstance, however trying, he would find him a steady and faithful friend, and that his powerful and athletic form, and excellent constitution, had
never been surpassed. This person was a medical man, and was so confirmed in the opinion that Clapperton, from the strength of his constitution, could not fall a sacrifice to disease, that, until the arrival of Clapperton’s servant, Richard Lander, from his last and fatal expedition, he would not (like many more who knew Clapperton) believe the report of his death in any way but by accident.
In the highest spirits, Lieutenant Clapperton left Edinburgh, where he had been for a short time with his sister and other relations. Before his departure, he was introduced by Lady Seaforth (the mother of his friend Mackenzie) to a distinguished countryman, the author of the Man of Feeling. Clapperton’s spirits were elated, and he left Edinburgh and his relations with the highest hopes. He returned to England, and was made a commander in June 22, 1825; and before he could finish for the press an account of his former journey, he was engaged again, by Lord Bathurst, for a second mission, by the way of the western coast of Africa, near the Bight of Benin. He sailed from Portsmouth in his Majesty’s sloop Brazen, commanded by Captain Willis; and was accompanied by Doctor Dickson, Captain Pearce, and Doctor Morrison. They called at Sierra Leone; from that to Benin, where they landed; but Dr. Dickson landed near Whida, and proceeded by the way of Dahomy. Captains Clapperton, Pearce, and Dr. Morrison, pushed their way up the country; but they were soon attacked with disease, and Captain Pearce and Doctor Morrison died, as did also Columbus, the former servant of Lieut.-Col. Denham. Captain Clapperton and his servant, Richard Lander, accompanied by Mr Houtson, a British resident at Benin, proceeded across the mountains to Katunga, where Mr. Houtson left them to return to the coast, where he shortly afterwards died. Dr. Dickson reached Dahomey, and proceeded on his way to join Clapperton, but has not since been heard of. Captain Clapperton, with his servant, Lander, and a native black of Houssa, reached Soccatoo in safety, where they remained many months; but at last the captain was seized with a fever and dysentery, which terminated his existence, and was buried, by his faithful servant, four miles south-east of Soccatoo, at a village called Chungary, April 13, 1827.
Thus perished, in the bloom of life, an officer beloved and respected by those of his profession who were acquainted with him; a man of a daring and enterprising spirit; and one who, for humanity and active benevolence, could be surpassed by none.
INTRODUCTION.
W the late Captain Clapperton made his way to Soccatoo for the first time, in the year 1824, he received the most flattering attentions, and every mark of kindness, from Bello, the sultan of the Fellans, as they call themselves, or Fellatas, as they are called by the people of Soudan. This chieftain may be said to rule over almost the whole of that part of North Africa which is distinguished by the name of Houssa, though he appears to have lost a considerable portion of what his father, Hatman Danfodio, first overran; and many of the petty chiefs still continue in a state of rebellion, some of them within a day’s journey of his capital. In the course of frequent conversations held with this chief, at his usual residence of Soccatoo, Clapperton was given to understand, that the establishment of a friendly intercourse with England would be most agreeable to him; that he wished particularly for certain articles of English manufacture to be sent out to him to the sea-coast, where there was a place of great commerce belonging to him, named Funda: he also expressed a wish that an English physician and a consul should be appointed to reside at another sea-port, called Raka; to the former of which places, he said, he would despatch messengers to bring up the articles from England; and to the latter he would send down a proper person to transact all matters of business between the two governments, through the intervention of the English consul; and he made no difficulty in declaring his readiness to adopt measures for putting an entire stop to that part of the slave-trade supposed to be carried on by his subjects with foreigners.
On the arrival of Clapperton in England, Lord Bathurst, then secretary of state for the colonies, considering this so favourable an
opportunity of establishing an intercourse with the interior of Africa, and probably of putting an effectual check, through this powerful chief, to a large portion of the infamous traffic carried on in the Bight of Benin, and also for extending the legitimate commerce of Great Britain with this part of Africa, and at the same time adding to our knowledge of the country, did not hesitate in adopting the arrangement which Clapperton had made with Bello. Accordingly it was determined to send him out again to that chief, by the way of Benin, with suitable companions and presents, in order that a communication might be opened between Soccatoo and the seacoast, and an attempt made to carry into effect the objects to which Bello was supposed to have given his hearty assent.
It had been arranged that, after a certain period agreed upon, Bello should send down his messengers to Whidah, on the coast, to meet Captain Clapperton and his companions. On their arrival, however, in the Bight of Benin, they could neither gain any intelligence of Bello’s messengers, nor did any of the people there know any thing of such names as Funda or Raka, the places which were pointed out by Bello as lying on the sea-coast. The country of Houssa, however, was well known by name, and as the precise geographical position of Soccatoo had been ascertained, our enterprising travellers could have no difficulty in knowing what direction to take; but the spot from whence it would be most advisable to start was a point not so easily to be determined. They finally, however, selected Badagry, for reasons that will be briefly stated; and proceeding northerly, from one chief to another, the survivors met with some delay, but no serious impediments, in reaching the spot of their destination.
The conduct, however, of Bello, though at first kind, was afterwards changed to every thing the reverse, for reasons which will appear in the course of the journal. His desire for establishing an amicable intercourse was not even hinted at, nor one word respecting the physician, the consul, or the slave-trade; and, either through ignorance or design (the former, in all probability), Bello had totally misled Clapperton as to the position of the city or district of Funda; which, instead of being on the sea-coast, as stated by him, is
now ascertained to be at least 150 miles from the nearest part of the coast; and the other city, Raka, still farther in the interior. Indeed, one would almost suspect that Clapperton, from not being sufficiently acquainted with the Fellata language, must have mistaken the meaning of Bello on his former visit, had not the letter in Arabic, which he brought home from the latter, addressed to the king of England, borne him out in his representation of the proposals made or assented to by this chieftain. In this letter he says, “We agreed with him upon this (the prohibition of the exportation of slaves), on account of the good which will result from it, both to you and to us; and that a vessel of yours is to come to the harbour of Raka, with two cannons, and the quantities of powder, shot, &c. which they require, as also a number of muskets: we will then send our officer to arrange and settle every thing with your consul, and fix a certain period for the arrival of your merchant ships; and when they come, they may traffic and deal with our merchants. Then, after their return, the consul may reside in that harbour (namely, Raka) as protector, in company with our agent there, if God be pleased.”
It is clear, from this letter, that Bello understood what was proposed and accepted, but, with regard to the geographical position of his two sea-ports, he was evidently most grossly ignorant; for, admitting the ambiguity of the Arabic word bahr, which signifies any great collection of water, whether sea, lake, or river, merchant ships could not get up to Raka, which is an inland town, not situated on any coast or river. Be this as it may, an expedition, as already stated, was planned without loss of time, at the head of which Clapperton was placed. He was allowed to take with him, as a companion, a fellow-countryman of the name of Dickson, who had been brought up as a surgeon, in which capacity he had served in the West Indies, but had recently been studying the law. This person considered himself to be inured to a tropical climate, and was supposed to have a sufficient knowledge of medicine to take care of himself and the rest of the party.
In an enterprise of this novel and hazardous nature, it was deemed advisable to unite two other gentlemen to those abovementioned; in order that, when once at Soccatoo, two of them might
be spared to set out from thence, and explore the country of Soudan in various directions. For this purpose, Captain Pearce of the navy, and Dr. Morrison, a naval surgeon, were selected; the former an active and accomplished officer, and a most excellent draughtsman; the latter well versed in various branches of natural history. Unhappily, it was not their good fortune to live long enough to put their respective talents in practice for the benefit of the public, or the gratification of their friends; having each of them, on the same day, fallen a sacrifice to the pestilential climate, at a very early period of their journey in Africa.
The presents intended for the Sultan of the Fellatas, and also for the Sheik of Bornou, being all ready, the four gentlemen, with their servants, embarked in his majesty’s ship Brazen on the 27th August, 1825, and, after touching at Teneriffe and St. Jago, arrived in the Bight of Benin on the 26th November, 1825. Mr. Dickson being desirous of making his way alone to Soccatoo, for what reason it does not appear, was landed at Whidah, where a Portuguese gentleman, of the name of De Sousa, offered to accompany him as far as Dahomey, where he had resided for some time in the employ of the king. The offer was accepted, and Dickson, taking with him a mulatto of the name of Columbus, who had been a servant to Lieutenant-Colonel Denham on the former expedition to Bornou, departed on the 26th November, arrived safe at Dahomey, where he was well received, and sent forward to a place called Shar, seventeen days’ from Dahomey, under a suitable escort, where he also arrived safely, and had an escort given him from thence on his intended journey to Youri, since which no account of him whatever has been received. By some Dahomey messengers, which Clapperton met with at Wawa, he sent a letter to Dickson; but it is evident they did not fall in with him, as the letter was some months afterwards sent down to the coast. It may here be observed, that though Whidah was the port to which Bello was ultimately understood to say he would despatch his messengers to convey the travellers, and their presents and baggage, to Soccatoo, it did not appear that any inquiries had been made there respecting them; nor did any person there seem to know more about Bello or Soccatoo, than was known, further on, of Funda or Raka.
